Transcript Wernicke`s Aphasia

Lesion Localization in Neuroradiology:
Classic Neurologic Exam and
Neuroimaging Correlates
eEdE-07
John A. Coburn, MD
Samuel I. Frost, DO
Tabassum A. Kennedy, MD
John-Paul J. Yu, MD, PhD
Department of Radiology
Department of Radiology
University
of Wisconsin School of Medicine and Public Health
University of Wisconsin School of Medicine and Public Health
Disclosures
• None of the authors have
any financial disclosures.
• All diagrams used in this
exhibit were created by the
authors.
Department of Radiology
University of Wisconsin School of Medicine and Public Health
Objectives
• Many pathologic processes affect the central nervous system in
characteristic anatomic locations, producing predictable neurologic
examination findings.
• An understanding of common neurologic presentations can help
the neuroradiologist target their search pattern and hone in on
pathology that may otherwise go undetected.
• In this exhibit, we highlight key neuroanatomic landmarks in a
case-based format using lesions characteristically affecting these
locations and their corresponding classic clinical presentation. A
discussion regarding the functional anatomy of the neuroanatomic
landmark of interest follows each case.
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University of Wisconsin School of Medicine and Public Health
Case Contents
Anatomy Review
Gelastic Seizure
Upper Extremity
Sensory Deficit
Palatal Myoclonus
Upper Extremity
Motor Deficit
Confusion, Ataxia &
Vision Change
Fluent Aphasia
Double Vision &
Facial Weakness
Expressive Aphasia
Dysarthria & Gait
Disturbance
Focal Visual Deficit
Vertigo & Crossed
Hemisensory Deficits
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each box
to view
each case
Key Neuroanatomy: Lateral Convexity
Parietal Lobe
Frontal Lobe
Occipital
Lobe
Temporal Lobe
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Key Neuroanatomy: Lateral Convexity
Precentral
sulcus
Central sulcus
Postcentral
sulcus
Parieto-occipital
fissure
SMG
AG
Superior frontal
sulcus
PT
POP
POR
Inferior frontal
sulcus
Lateral sulcus
Superior
Temp. sulcus
Intraparietal
sulcus
Middle Temp
sulcus
SMG Supramarginal gyrus; AG Angular gyrus; POR Pars orbitalis; PT Pars triangularis; POP Pars opercularis
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AHR Anterior horizontal ramus of the lateral
sulcus;
AAR
Anterior
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of Wisconsin
School
of Medicine ascending
and Public Health ramus of the lateral sulcus
Key Neuroanatomy: Axial Vertex
Superior
frontal sulcus
Superior frontal
gyrus
Middle frontal
gyrus
Inferior frontal
gyrus
Inferior frontal
sulcus
Precentral sulcus
Central sulcus
Postcentral sulcus
Supramarginal
gyrus
Lateral sulcus
Superior Temp
sulcus
Angular gyrus
Intraparietal
sulcus
Occipital gyri
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Key Neuroanatomy: Midline Sagittal
Central sulcus
Ascending ramus of
the cingulate sulcus
Parieto-occipital
sulcus
Paracentral
lobule
Cingulate sulcus
Precuneus
Cingulate gyrus
Cuneus
Fornix
Parolfactory
area
Lingual gyrus
Interthalamic adhesion
Collateral sulcus
Inferior temporal sulcus
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Calcarine fissure
78 F with headache and focal left upper extremity
sensory deficits
T1
T1+C
FLAIR
HPI: 78 yo woman presents with gradual onset of headaches and
extremity sensory changes that appear to be localized to her left
upper extremity
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78 F with headache and focal left upper extremity
sensory deficits
T1
FLAIR
T1+C
Central sulcus
Post central
gyrus
Axial T1, post contrast axial T1 and FLAIR images at the level of
frontoparietal vertex demonstrate a focal enhancing mass along the right
post central gyrus with associated vasogenic edema (blue arrow). The
mass was dural based, resected and consistent with a meningioma.
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Sensorimotor Cortex
The central sulcus is an important sulcus which
divides the primary cortex (precentral gyrus)
within the frontal lobe from the primary sensory
cortex (post central gyrus) within the parietal
lobe.
Superior frontal sulcus
Precentral sulcus
Central sulcus
Postcentral sulcus
Pars Marginalis
Precentral gyrus
Postcentral gyrus
Identifying the central sulcus:
1) The sagittally oriented superior frontal
sulcus (which divides the superior frontal
gyrus from the middle frontal gyrus)
terminates within the precentral sulcus. The
sulcus immediately posterior to the
precentral sulcus is typically the central
sulcus.
2) The central sulcus is the main sulcus that
extends to the midline.
3) The pars marginalis or “pars bracket sign” is
a paired short sulcus immediately posterior
to the central sulcus.
4) Identify the “hand knob”. U shaped
segment of the precentral gyrus
corresponding to upper extremity motor
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56 M with right upper extremity weakness
CT
DWI
ADC
FLAIR
HPI: 56 yo male who presents with the acute onset of right upper
extremity weakness which began 4 hours prior to presentation. A
stroke was suspected and a stroke code was activated.
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56 M with right upper extremity weakness
CT
DWI
ADC
FLAIR
Hand Knob
Axial CT at the level of the vertex demonstrates no hemorrhage or
evidence for cytotoxic edema. An MR was subsequently performed
which demonstrates a small focus of diffusion restriction consistent
with infarction (red arrow) within the left precentral gyrus colocalizing to the “hand knob” on the homunuclus (blue arrow).
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55 M with fluent aphasia
DWI
FLAIR
HPI: A 55 year old male presents with acute onset speech difficulty.
The evaluating neurologist states the patient’s speech deficits are
consistent with a fluent aphasia.
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55 M with fluent aphasia
DWI
FLAIR
Axial diffusion-weighted and sagittal T2-FLAIR images demonstrate
areas of restricted diffusion with associated T2-FLAIR hyperintense
signal involving the left posterior superior temporal (STG) and
supramarginal gyri (SMG), consistent with early subacute infarct.
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Wernicke’s Aphasia
SMG
AG
Wernicke’s area (outlined in green) refers to
the dominant (left) hemispheric posterior
perisylvian region, including the posterior
superior temporal gyrus and supramarginal
gyrus (SMG). The angular gyrus (AG) is
located posterior to the SMG.
Lesions involving Wernicke’s area
lead to speech errors known as
phonemic paraphasic errors, in
which the phonemes (consonant
or vowel sounds distinguishing
one word from a different but
similar word) are chosen
incorrectly. These errors are
cardinal features of Wernicke’s
aphasia, a type of fluent aphasia.
Wernicke’s area was classically
thought to be involved in speech
comprehension, although modern
evidence indicates a role in
speech production, including
phonologic retrieval, as well as the
monitoring, feedback and
correction of self-produced
speech.
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26 M with expressive aphasia
T2
T1+C
FLAIR
HPI: A 26 year old male presents with gradual onset speech
difficulty. The evaluating neurologist states the patient’s speech
deficits are consistent with an expressive aphasia.
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26 M with expressive aphasia
T2
PT
Insula
T1+C
FLAIR
POP
POP
PT
Insula
Axial T2, sagittal T1 post contrast and coronal FLAIR MR images of the
brain demonstrate an expansile T2/FLAIR hyperintense non enhancing
mass involving the left pars triangularis (PT) and pars opercularis (POP)
of the left inferior frontal gyrus as well as the insula. The mass was
resected and pathology was consistent with an oligodendroglioma.
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Broca’s aphasia
AAR
IFS
AHR
PCS
Broca’s area
POP
POP
POR
PT
PT
POR
Broca’s area refers to the pars triangularis (PT) and pars opercularis (POP)
of the dominant (typically left) inferior frontal gyrus. The pars orbitalis
(POR), PT and POP comprise the inferior frontal gyrus. The POR is
separated from the PT by the anterior horizontal ramus (AHR) of the lateral
sulcus. The anterior ascending ramus (AAR) of the lateral sulcus separates
PT from POP. [IFS = inferior frontal sulcus; PCS = inferior extent of the
precentral sulcus]
Broca’s area is involved in the motor component of speech production.
Broca’s aphasia is an expressive aphasia characterized by non-fluent,
scarce production of speech, with poor articulation in the form of short
sentences with only a few words.
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PT
POP
69 M with visual field deficit and confusion
FLAIR
DWI
TOF
HPI: A 69 yo male presents with acute onset of visual disturbance and
confusion.
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69 M with visual field deficit and confusion
FLAIR
DWI
TOF
Sagittal FLAIR, axial diffusion and time of flight MRA of the posterior
circulation demonstrate cytotoxic edema within the lingual gyrus of the left
occipital lobe and medial left temporal lobe (blue arrows) consistent with an
infarction within the posterior cerebral artery (PCA) distribution related to
occlusion of the left P1 segment (red arrow).
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Visual Field Deficits
Parieto-occipital
sulcus
Cuneus
Calcarine
fissure
Lingual gyrus
Lingual gyrus
The occipital lobe, the primary visual cortex, is separated
from the parietal lobe by the parieto-occipital sulcus. The
calcarine fissure divides the occipital lobe into 2 primary
lobes, the cuneus and the lingual gyrus.
Opto-retinal mapping is maintained along the visual
pathway. The right and left occipital lobes receive
temporal and nasal input from each eye. The input below
the equator is mapped to the cuneus and above the
equator is mapped to the lingual gyrus.
R
L
The visual field deficit in this patient with an
infarct involving the left lingual gyrus
corresponds to a right superior quadrantanopia.
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30 M with gelastic seizures
T1
T1 +C
FLAIR
HPI: A 30 year old male is been treated for chronic, medically refractory
epilepsy. One of his seizure types consists of a rising epigastric
sensation, followed by the development of giggling or staring.
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30 M with gelastic seizures
T1
T1 +C
FLAIR
Sagittal precontrast T1, coronal post contrast and coronal FLAIR
images demonstrate a well circumscribed T1 isointense, T2/FLAIR
mildly hyperintense, nonenhancing lobular mass arising from the
left inferior aspect of the tuber cinereum (blue arrow).
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Tuber cinereum hamartoma – Gelastic seizures
Normal Comparison
Mamillary
Body
Hamartoma
Optic Chiasm
Tuber Cinereum
of Hypothalamus
The tuber cinereum is an eminence of gray matter on the lower aspect of the hypothalamus,
bordered anteriorly by the optic chiasm and posteriorly by the mammillary bodies. It forms
part of the floor of the third ventricle, and its lower surface is the root of the pituitary
infundibulum.
Tuber cinereum hamartomas are congenital tumors composed of neurons organized in
poorly demarcated clusters that serve as a direct epileptogenic focus. The hypothalamus
plays an important role in the mediation of emotional responses, although the specific reason
that tuber cinereum hamartomas are associated with gelastic (laughing) seizures is
incompletely understood.
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33 M with palatal myoclonus
T2
FLAIR
T2 *
T2 *
Case courtesy of Dr. Kelli Dawson, University of Wisconsin Hospitals and Clinics
HPI: A 33 year old male presents for follow up MR imaging after suffering
traumatic brain injuries 12 months prior. His previously documented
injuries include grade III diffuse axonal injury. The patient demonstrates
persistent symptoms of palatal myoclonus.
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33 M with palatal myoclonus
T2
FLAIR
T2 *
T2 *
Case courtesy of Dr. Kelli Dawson, University of Wisconsin Hospitals and Clinics
Axial T2 and sagittal T2-FLAIR images of the brainstem demonstrate hyperintensity
and enlargement of the right inferior olivary nucleus, consistent with hypertrophic
olivary degeneration (HOD) (blue arrows). Two adjacent slices from axial T2* GRE
sequence demonstrate focal hemosiderin deposition consistent with prior diffuse
axonal injury affecting the dorsal brainstem in the right central tegmental tract (orange
arrows), resulting in the HOD seen in the FLAIR sequences
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Hypertrophic olivary degeneration
FLAIR
FLAIR
RN
T2
FLAIR
RN
DN
ION
ION
DN
ION
Sequential coronal T2-FLAIR images from anterior to posterior (first 3 images from left to
right) demonstrate the dentato-rubro-olivary pathway (i.e. Guillain-Mollaret triangle),
comprised of the inferior olivary nucleus (ION), the ipsilateral red nucleus (RN), and the
contralateral dentate nucleus (DN), which in this case demonstrates abnormal signal due to
gliosis from prior tumor resection, resulting in HOD. Final image (far screen right)
demonstrates classic findings of high T2 signal and hypertrophy of the inferior olivary nuclei
seen in bilateral HOD.
The efferent fibers travel from the dentate nucleus to the contralateral red nucleus via the
superior cerebellar peduncle. The tract decends from the red nucleus to the ipsilateral inferior
olivary nucleus via the central tegmental tract. The afferent pathway originates from the
inferior olivary nucleus to the contralateral cerebellum. Disruption of the dentato-rubro-olivary
pathway affects the reflex arc that controls fine voluntary movements, and classically
presents with palatal myoclonus.
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41 F with confusion, ataxia, and vision changes
FLAIR
FLAIR
HPI: A 41 year old female with history of gastric bypass who “drinks
too much” (per her husband), presents with subacute onset global
confusion, marked bilateral lower extremity weakness, ataxia,
evidence of peripheral neuropathy, and recent onset blurred vision.
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41 F with confusion, ataxia, and vision changes
FLAIR
FLAIR
Axial T2-FLAIR images demonstrate hyperintense signal involving the
periaquedectal grey matter (blue arrow, banks of the third ventricle
(orange arrows) and mammillary bodies (white arrows).
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Wernicke’s Encephalopathy
Thiamine is a water soluble vitamin and
important cofactor for key enzymes in the Krebs
and pentose-phosphate cycles. Rapid depletion
can occur in those with poor nutrition,
particularly those with chronic alcoholism.
Wernicke’s encephalopathy (WE) classically
presents with the triad of altered
consciousness, ocular movement dysfunction
and ataxia. Other signs of nutritional deficiency,
such as polyneuropathy, can also occur.
MB
PAG
Thiamine deficiency leads to impaired cerebral energy
metabolism, focal lactic acidosis, and disruption of
cellular osmotic gradients, among other abnormalities,
which have a tendency to effect the periventricular and
periaqueductal regions, where thiamine-related glucose
and oxidative metabolism is abundant.
MR findings of T2 signal abnormality (with
diffusion restriction in the acute phase)
involving the periaqueductal grey matter, walls
of the third ventricle, mammillary bodies, with
variable involvement of the medial thalami,
caudate nuclei and frontal and parietal cortex is
typical. Abnormal post-contrast enhancement
involving the mammillary bodies,
periaqueductal grey matter and medial thalami
is another feature.
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32 F with double vision and facial weakness
FLAIR
T2
T1
HPI: A 32 year old female with history of multiple sclerosis presents with new
double vision and left facial weakness. On physical examination, the patient
has a left horizontal gaze palsy and dense left sided facial weakness
(including loss of forehead wrinkling and left facial droop) consistent with
lower motor neuron deficits referable to left cranial nerves VI and VII.
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32 F with double vision and facial weakness
FLAIR
T2
T1
Sagittal T2-FLAIR, axial T2 and T1 weighted images at the level of the pons
demonstrate a lesion that is T2/FLAIR hyperintense (white arrow) and T1
hypointense (orange arrow) involving the left facial colliculus, consistent with
a demyelinating lesion in this patient with known multiple sclerosis.
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Facial colliculus syndrome
VI
VI
VII
VII
Pons
The facial colliculi are paired small elevations (blue arrows) protruding from the dorsal pons
into the fourth ventricle. They are formed by motor fibers from the facial nerve nucleus
curving backward and laterally around the posterior aspect of the abducens nucleus prior to
joining parasympathetic and special sensory fibers of the facial nerve and assuming an
anterolateral course in the caudal pons.
A lesion affecting the facial colliculus will cause deficits of the abducens nerve and motor
fibers of the facial nerve, leading to ipsilateral CN VI and VII palsies, manifesting as
ipsilateral horizontal gaze palsy and lower motor neuron pattern facial weakness. This
presentation has been termed the “facial colliculus
syndrome”.
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66 F with dysarthria and gait disturbance
T2
HPI: A 66 year old female being treated for pseudomembranous
colitis developed new onset dysarthria and ataxia. Her medication
list included metronidazole for treatment of her infection.
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66 F with dysarthria and gait disturbance
T2
An axial T2-weighted image at the level of the brainstem and
cerebellum demonstrates symmetric hyperintense signal in the
dentate nuclei of the cerebellar hemispheres bilaterally (arrows).
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66 F with dysarthria and gait disturbance
T2
T2
The abnormal signal on T2-weighted images resolved after removal of
the offending medication.
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Dentate nucleus– Metronidazole neurotoxicity
Medulla
Dentate
The paired dentate nuclei of the cerebellum appear to
have anatomically separate, functionally distinct
motor and non-motor domains. The dorsal dentate
projects to cortical areas involved in coordination and
control of motor activity, the ventral dentate projects
to premotor and posterior parietal areas thought to be
involved in higher cognitive and visuospatial
functions.
Metronidazole neurotoxicity-induced encephalopathy
is a rare complication of metronidazole use. The
clinical presentation of reported cases shows
commonalities such as dysarthria and gait
disturbance, with other variable features such as
extremity weakness.
Midbrain
Splenium
Normal axial FLAIR images at the level of the medulla,
dentate nuclei, midbrain and splenium demonstrating
common areas of involvement in metronidazole toxicity,
including the dorsal medulla (white arrowheads), dentate
nuclei, red nuclei, periaqueductal gray, and splenium.
MR findings include T2-FLAIR hyperintense signal
almost always involving the dentate nuclei, with other
commonly affected areas including the midbrain
(tectum, red nucleus, and tegmentum around
periaqueductal gray matter), dorsal pons (the
vestibular nucleus, superior olivary nucleus, and the
abducens nucleus), dorsal medulla, and corpus
callosum (splenium). These lesions are always
bilateral and symmetric.
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41 M with vertigo and crossed hemisensory deficits
T1
DWI
HPI: A 41 year old male presents with nausea and vomiting, vertigo, right
face tingling, and clumsiness of the right hand. Physical examination
demonstrates right arm dysmetria, and right face and left body
hemisensory changes.
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41 M with vertigo and crossed hemisensory deficits
T1
DWI
Axial pre-contrast T1-weighted and DWI images demonstrate a focus of
restricted diffusion in the right dorsolateral medulla (red arrow), consistent
with acute infarct. There is crescentic, intrinsically T1 hyperintense signal in
the right vertebral artery (blue arrow), consistent with intramural hematoma
related to a vascular dissection.
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Lateral medullary (Wallenberg) syndrome
Wallenberg syndrome is caused by an infarct of the
lateral medulla due to compromise of the posterior inferior
cerebellar artery (PICA). In younger patient’s this is
commonly caused by vertebral artery dissection with
secondary compromise of PICA. In older patient’s this
can be caused by thromboembolic disease.
Classically, patient’s with Wallenberg syndrome present
with a Horner syndrome (ipsilateral ptosis, miosis and
anhydrosis), ipsilateral ataxia, and ipsilateral face and
contralateral body sensory changes (so-called “crossed
hemisensory deficits”), but they may present with varying
combinations of deficits referable to the lateral medulla.
Vertebral
artery
The clinical presentation is due to involvement of a
combination of nuclei and tracts in the dorsolateral
medulla. Involvement of descending sympathetic tracts
PICA
leads to Horner’s syndrome. Involvement of the inferior
cerebellar peduncle and spinal trigeminal nucleus/tracts
leads to ipsilateral cerebellar signs and facial sensation
deficits, respectively. Contralateral hemibody
pain/sensory deficits are due to involvement of the spinal
lemniscus (ie spinothalamic) tracts, which decussate at
the level of the spinal cord prior to ascending into the
Commonly affected: Spinal lemniscus, spinal
trigeminal nucleus, tract of spinal trigeminal nucleus,
medulla. Variable involvement of the vestibular nuclei and
inferior cerebellar peduncle
nucleus ambiguus may lead to symptoms of vertigo and
Occasionally affected: Dorsal vagal nucleus, nucleus Department
of Radiology
dysarthria/dysphagia,
etc.
solitarius, vestibular nuclei, nucleus ambiguus
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Summary
• Knowing the clinical history
can aid in the detection of
pathology on neuroimaging
studies.
• A firm understanding of
neuroanatomy and important
imaging landmarks can allow
the radiologist to precisely
localize and characterize
pathology.
Department of Radiology
University of Wisconsin School of Medicine and Public Health
Sup. parietal lobule
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Department of Radiology
University of Wisconsin School of Medicine and Public Health