Benedict Syndrome
Content
Benedict syndrome
Sindrom otak tengah mempengaruhi saraf cranial III (Nervus Occulomotorius),
Red Nukleus, dan Pedunkel, menyebabkan hemiparesis kontralateral dengan
tremor di extremitas yang parese dan kelumpuhan ipsilateral occulomotorius.
Defisit occulomotorius termasuk ptosis, strabismus divergen, dan dilatasi pupil.
Red nucleus berkoordinasi dari jaras cerebelar thalamic ke cereberel pedunkel
superior (brachium conjunctivum). Lesi di red nucleus menghasilkan deficit
dalam berkoordinasi kontralateral (ataxia), dysmetria, dysdiadokokinesis, rubral
tremor ( resting tremor kasar yang meningkat apabila bergerak), dan
pseudoparkinson tremor. Terkadang, sindrom ini mempengaruhi lemniskus
medialis atau traktus spinothalamicus, dengan defisit sensorik kontralateral.
Weber's syndrome
Struktur penting yang terlibat descending kortikospinal dan kortikobulbar di
cerebral pedunkel, and serat nervus III yang menyebrangi pedunkel di midbrain.
Apabila lesi di sebelah kanan, pasien akan mengalami hemiparesis kiri dan parese
N III kanan (ptosis, tidak dapat menggerakan mata keatas, kebawah, atau medial,
dan dilatasi pupil (Jika jaras dari nukleus Ediger-Westphal ikut terlibat)
Benedikt and "plus-minus lid" syndromes arising from posterior
cerebral artery branch occlusion.
J Neurol Sci. 2005; 228(1):105-7 (ISSN: 0022-510X)
Akdal G; Kutluk K; Men S; Yaka E
Department of Neurology, Faculty of Medicine, Dokuz Eylül University, 35340,
Inciralt, Izmir, Turkey. [email protected]
A 53-year-old man was admitted with diplopia, right ptosis, left lid retraction, mild left
sided weakness and involuntary movements. Neurological examination revealed
plus-minus lid and Benedikt's syndromes together. Magnetic resonance imaging
(MRI) showed two distinct mesencephalic infarctions in territories of paramedian and
pedincular perforating arteries. Magnetic resonance angiography (MRA) showed
severe stenosis of proximal segment of the right posterior cerebral artery (PCA).
Rare clinical presentations such as Benedikt and plus-minus syndromes can be seen
together and be due to stenosis of the posterior cerebral artery with specific regional
infarctions.
Ischemic infarction in the territory of the PCA is usually secondary to total occlusion of
the vessel.2 The clinical features vary and may include pure hemianopsia,2 resemble
middle cerebral artery occlusion,3 4 or be restricted to thalamic disturbances.5 Symptoms
of PCA stenosis are uncommon. Pessin et al1 reported the first series of patients with
angiographically proven PCA stenosis. The major clinical features were transient
ischemic attacks with contralateral visual symptoms and, in some patients, contralateral
sensory symptoms. Only two of the six patients had permanent neurological deficits, and
in both patients they were contralateral visual field disturbances.
Our patient is unique because only brain stem symptoms were present. Symptoms of
medial temporal and occipital lobe ischemia were absent. Ipsilateral oculomotor nerve
palsy and contralateral ataxia and corticospinal tract findings are consistent with
Benedikt's syndrome.6 Previous reports of Benedikt's syndrome6 did not establish an
arterial pathology. Our patient with signs of Benedikt's syndrome had clear midbrain
infarction with involvement of red nucleus, cerebral peduncle, oculomotor fascicles, and
lower oculomotor nucleus shown by MRI. Multiple small, peduncular arterial branches
arise from the proximal PCA and immediately penetrate the ipsilateral cerebral peduncle
to supply the corticospinal and corticobulbar tracts, substantia nigra, red nucleus, third
and fourth cranial nerve nuclei, and other ipsilateral midbrain structures.7 Our patient's
high-grade PCA peduncular segment stenosis visualized by vertebral arteriogram likely
resulted in origin occlusion of several of these small, penetrating branches and subsequent
midbrain infarction. MRI demonstrated midbrain sparing at the level of the upper superior
colliculus and Edinger-Westphal nucleus, thus preserving pupillary parasympathetic
innervation. While highly stenotic, the PCA remained patent with sparing of more distal
brain territories.
Later in this patient's course, the pupillary function became normal, even though a
complete external oculomotor nerve palsy persisted. Previous reports of pupil-sparing
oculomotor nerve palsy8 9 have established that intra-axial midbrain infarction similar to
that in this patient may have been responsible. This report establishes PCA stenosis as one
type of arterial pathology responsible for the syndrome.
The clinical features of this patient provide additional symptoms to the syndrome of PCA
stenosis, and their recognition may hasten the diagnosis of PCA stenosis and appropriate
treatment.
Syndrome
Site of lesion
Weber
(hemiparesis alternans
oculomotoria)
Benedikt
Ipsilateral
side
Contralateral side
Oculomotor palsy
Hemiparesis
Oculomotor palsy
Hyperkinesis
(athetosis,chorea)
Rigor
Disturbance of deep
sensibility
Named Brainstem Syndromes
Eponym
Site
Weber
Base of
Midbrain
Claude
Midbrain
Cranial
Nerves
Tracts
Signs
Usual Cause
III
Corticospinal
Oculomotor
palsy with
crossed
hemiplegia
Vascular, tumor
III
Red nucleus and Oculomotor
Vascular, tumor
tegmentum
Benedict
Midbrain
III
tegmentum
Nothnagel
Midbrain
tectum
Parinaud
Brachium
Conjunctivum
palsy with
contralateral
cerebellar ataxia
and tremor
Red nucleus,
corticospinal
tract, brachium
conjunctivum
Oculomotor
palsy,
Vascular,
contralateral
tuberculoma,
cerebellar ataxia,
tumor
corticospinal
signs
Superior
Unilateral or
cerebellar
bilateral III
peduncles
Paralysis of
upward gaze and
accommodation, Pinealoma,
fixed pupils,
hydrocephalus
retraction
nystagmus
Dorsal
Midbrain
MillardGubler and Base of
Raymond- Pons
Foville
Ocular palsies,
paralysis of
Tumor
gaze, cerebellar
ataxia
VII and
sometimes
VI
Corticospinal
tract
Facial and 6th
palsy,
contralateral
Vascular,tumor
hemiplegia,
sometimes gaze
palsy
Avellis
Medulla
X
tegmentum
Paralysis of soft
Spinothalamic, palate and vocal
Infarct or
sometimes
cord and
Tumor
pupillary fibers contralateral
hemianesthesia
Jackson
Medulla
X,XII
Tegmentum
Corticospinal
Avellis plus
ipsilateral
tongue
Lateral
STT,Descending
Pupil fibers,
Spinocerebellar
and
olivocerebellar
tracts
Ipsi V, IV, X, XI
palsy, Horner's,
Vascular - Pica
cerebellar ataxia.
or vertebral
Contra pain and
temp
Medulla,
Spinal
Wallenberg lateral
V,IV,X,XI
tegmentum
Infarct or
Tumor
SINDROMA BENEDIKT
DISUSUN OLEH
ALDI BESTARY SITUNGKIR
00-028
PEMBIMBING
DR TUMPAL SIAGIAN Sp.S
KEPANITRAAN KLINIK NEUROLOGI
PERIODE 26 MARET-28 APRIL 2007
FAKULTAS KEDOKTERAN
UNIVERSITAS KRISTEN INDONESIA
JAKARTA
Sindrom otak tengah mempengaruhi saraf cranial III (Nervus Occulomotorius),
Red Nukleus, dan Pedunkel, menyebabkan hemiparesis kontralateral dengan
tremor di extremitas yang parese dan kelumpuhan ipsilateral occulomotorius.
Defisit occulomotorius termasuk ptosis, strabismus divergen, dan dilatasi pupil.
Red nucleus berkoordinasi dari jaras cerebelar thalamic ke cereberel pedunkel
superior (brachium conjunctivum). Lesi di red nucleus menghasilkan deficit
dalam berkoordinasi kontralateral (ataxia), dysmetria, dysdiadokokinesis, rubral
tremor ( resting tremor kasar yang meningkat apabila bergerak), dan
pseudoparkinson tremor. Terkadang, sindrom ini mempengaruhi lemniskus
medialis atau traktus spinothalamicus, dengan defisit sensorik kontralateral.
Weber's syndrome
Struktur penting yang terlibat descending kortikospinal dan kortikobulbar di
cerebral pedunkel, and serat nervus III yang menyebrangi pedunkel di midbrain.
Apabila lesi di sebelah kanan, pasien akan mengalami hemiparesis kiri dan parese
N III kanan (ptosis, tidak dapat menggerakan mata keatas, kebawah, atau medial,
dan dilatasi pupil (Jika jaras dari nukleus Ediger-Westphal ikut terlibat)
Benedikt and "plus-minus lid" syndromes arising from posterior
cerebral artery branch occlusion.
J Neurol Sci. 2005; 228(1):105-7 (ISSN: 0022-510X)
Akdal G; Kutluk K; Men S; Yaka E
Department of Neurology, Faculty of Medicine, Dokuz Eylül University, 35340,
Inciralt, Izmir, Turkey. [email protected]
A 53-year-old man was admitted with diplopia, right ptosis, left lid retraction, mild left
sided weakness and involuntary movements. Neurological examination revealed
plus-minus lid and Benedikt's syndromes together. Magnetic resonance imaging
(MRI) showed two distinct mesencephalic infarctions in territories of paramedian and
pedincular perforating arteries. Magnetic resonance angiography (MRA) showed
severe stenosis of proximal segment of the right posterior cerebral artery (PCA).
Rare clinical presentations such as Benedikt and plus-minus syndromes can be seen
together and be due to stenosis of the posterior cerebral artery with specific regional
infarctions.
Ischemic infarction in the territory of the PCA is usually secondary to total occlusion of
the vessel.2 The clinical features vary and may include pure hemianopsia,2 resemble
middle cerebral artery occlusion,3 4 or be restricted to thalamic disturbances.5 Symptoms
of PCA stenosis are uncommon. Pessin et al1 reported the first series of patients with
angiographically proven PCA stenosis. The major clinical features were transient
ischemic attacks with contralateral visual symptoms and, in some patients, contralateral
sensory symptoms. Only two of the six patients had permanent neurological deficits, and
in both patients they were contralateral visual field disturbances.
Our patient is unique because only brain stem symptoms were present. Symptoms of
medial temporal and occipital lobe ischemia were absent. Ipsilateral oculomotor nerve
palsy and contralateral ataxia and corticospinal tract findings are consistent with
Benedikt's syndrome.6 Previous reports of Benedikt's syndrome6 did not establish an
arterial pathology. Our patient with signs of Benedikt's syndrome had clear midbrain
infarction with involvement of red nucleus, cerebral peduncle, oculomotor fascicles, and
lower oculomotor nucleus shown by MRI. Multiple small, peduncular arterial branches
arise from the proximal PCA and immediately penetrate the ipsilateral cerebral peduncle
to supply the corticospinal and corticobulbar tracts, substantia nigra, red nucleus, third
and fourth cranial nerve nuclei, and other ipsilateral midbrain structures.7 Our patient's
high-grade PCA peduncular segment stenosis visualized by vertebral arteriogram likely
resulted in origin occlusion of several of these small, penetrating branches and subsequent
midbrain infarction. MRI demonstrated midbrain sparing at the level of the upper superior
colliculus and Edinger-Westphal nucleus, thus preserving pupillary parasympathetic
innervation. While highly stenotic, the PCA remained patent with sparing of more distal
brain territories.
Later in this patient's course, the pupillary function became normal, even though a
complete external oculomotor nerve palsy persisted. Previous reports of pupil-sparing
oculomotor nerve palsy8 9 have established that intra-axial midbrain infarction similar to
that in this patient may have been responsible. This report establishes PCA stenosis as one
type of arterial pathology responsible for the syndrome.
The clinical features of this patient provide additional symptoms to the syndrome of PCA
stenosis, and their recognition may hasten the diagnosis of PCA stenosis and appropriate
treatment.
Syndrome
Site of lesion
Weber
(hemiparesis alternans
oculomotoria)
Benedikt
Ipsilateral
side
Contralateral side
Oculomotor palsy
Hemiparesis
Oculomotor palsy
Hyperkinesis
(athetosis,chorea)
Rigor
Disturbance of deep
sensibility
Named Brainstem Syndromes
Eponym
Site
Weber
Base of
Midbrain
Claude
Midbrain
Cranial
Nerves
Tracts
Signs
Usual Cause
III
Corticospinal
Oculomotor
palsy with
crossed
hemiplegia
Vascular, tumor
III
Red nucleus and Oculomotor
Vascular, tumor
tegmentum
Benedict
Midbrain
III
tegmentum
Nothnagel
Midbrain
tectum
Parinaud
Brachium
Conjunctivum
palsy with
contralateral
cerebellar ataxia
and tremor
Red nucleus,
corticospinal
tract, brachium
conjunctivum
Oculomotor
palsy,
Vascular,
contralateral
tuberculoma,
cerebellar ataxia,
tumor
corticospinal
signs
Superior
Unilateral or
cerebellar
bilateral III
peduncles
Paralysis of
upward gaze and
accommodation, Pinealoma,
fixed pupils,
hydrocephalus
retraction
nystagmus
Dorsal
Midbrain
MillardGubler and Base of
Raymond- Pons
Foville
Ocular palsies,
paralysis of
Tumor
gaze, cerebellar
ataxia
VII and
sometimes
VI
Corticospinal
tract
Facial and 6th
palsy,
contralateral
Vascular,tumor
hemiplegia,
sometimes gaze
palsy
Avellis
Medulla
X
tegmentum
Paralysis of soft
Spinothalamic, palate and vocal
Infarct or
sometimes
cord and
Tumor
pupillary fibers contralateral
hemianesthesia
Jackson
Medulla
X,XII
Tegmentum
Corticospinal
Avellis plus
ipsilateral
tongue
Lateral
STT,Descending
Pupil fibers,
Spinocerebellar
and
olivocerebellar
tracts
Ipsi V, IV, X, XI
palsy, Horner's,
Vascular - Pica
cerebellar ataxia.
or vertebral
Contra pain and
temp
Medulla,
Spinal
Wallenberg lateral
V,IV,X,XI
tegmentum
Infarct or
Tumor
SINDROMA BENEDIKT
DISUSUN OLEH
ALDI BESTARY SITUNGKIR
00-028
PEMBIMBING
DR TUMPAL SIAGIAN Sp.S
KEPANITRAAN KLINIK NEUROLOGI
PERIODE 26 MARET-28 APRIL 2007
FAKULTAS KEDOKTERAN
UNIVERSITAS KRISTEN INDONESIA
JAKARTA
