Anatomic Localization

Dr. Rene Punsalan

June 28, 2010

LEGEND
Normal text : lecture and recording
Italics : book
OUTL INE
Approach to Patient with Suspected Neurological Disease
Benefits of Localization
Steps in Localization
Levels of Localization
Abnormal Cerebral Function
APPROACH to PATIENT with SUSPECTED NEUROLOGICAL
DISEASE
Data Gathering
History
Physical Exam
Neurological Exam difference from Medicine
Anatomic Localization
Where is the lesion?
You need to localize the lesion first before
attempting to do an etiologic diagnosis.
Localization is not unique for Neurology. For
example, a patient with cardiac disease, you have to
know whether the right side or the left side of the
heart is involved or whether the atrium or the
ventricle is involved. It is just carried to a greater
complexity in Neurology than any other field of
Medicine.
Can be one specific location, be multifocal, or be pa rt
of a diffuse process
Etiologic diagnosis
What is the nature of the lesion?
BENEFITS of LOCALIZATION
Directs diagnostic work-up
A female patient comes in complaining of back pain
and some weakness of the legs. Resident orders a
lumbosacral spine film. Finding nothing, the r esident
sends px home. Two weeks later, the patient comes
back paraplegic. The patient also has a sharp sensory
level at umbilicus (at T10) which localizes the lesion
within 2-3 segments below this. A thoracic spine film
was requested and the film shows that the patient
has Potts disease, w/c compressed the spinal cord
level at T10. This was completely missed by a
lumbosacral spine film because it is too low. If the
resident were able to localize the lesion, the resident
could have ordered a thoracic spine film.
Limits the differential diagnosis
If the lesion is localized to the brain, all you have to
consider are brain diseases. You dont have to test
the patient for all known neurologic diseases (e.g.,
diseases of the spinal cord or PNS)
Guards against going straight to a specific etiologic
diagnosis
A patient complains of vertigo and a cluster of
symptoms pointing to the pons. A doctor may
immediately label this as multiple sclerosis especially

in a young female patient. But it is recommended

that you localise the lesion first. The doctor might
have missed other lesions involving the pons (e.g.,
an AV malformation in the pons).
In a patient with spastic paraparesis, you might
immediately label it as demyelinating disease
(mostly untrea table). If you localise it first to the
thoracic core, you will consider other differentials
(e.g., Vit B12 deficiency, multiple sclerosis), which
are treatable or treated differently.
The different diseases in the brain can produce the
same set of manifestations so long as it involves the
same particular spot/place in the nervous system
Deciding on a location rather than an etiology first
will help you avoid missing importan t differentials
due to lack of consid era tion
Estimates the ex tent of the lesion
A patient presents with hemiplegia of the face, arm
and leg. This is the syndrome of a lacunar infarction
and it points to a very small area that is strategically
placed in the opposite internal capsule. In contrast, a
patient with right hemiplegia with expressive
aphasia suggests a cortical lesion. The lesion is
localised in the left cerebral hemisphere involving
the Brocas area and the motor tracts (more
extensive).
May suggest the etiologic diagnosis
The clustering of signs and symptoms and specific
location of the lesion is sometimes s uggestive of the
etiologic diagnosis.
For example, a set of brainstem and long tract signs
refer to the lateral medulla. If you plot that against
the anatomy of the medulla, you will see that they
follow an area that corresponds to a vascular
territory. This suggests that the cause of that lesion
is vascular, suggesting a lateral medullary syndrome
most likely vascular in nature (Wallenbergs
syndrome). This is due to occlusion of posterior
inferior cerebellar artery which supplies the
posterolateral part of the medulla.
Another example: a combination of optic monocular
blindness and spastic paraparesis with a sharp
sensory level. These are optic neuritis and myelitis so
combining the two will be neuromyelitis or Devics
disease which is a form of multiple sclerosis.
STEPS in LOCALIZATION
Step 1 : List all abnormal neurologic signs
Get the signs from the neurological examination.
Step 2 : Determine all possible neuroanatomic correlates
per sign.
Step 3 : Find the intersection.
Find the point wherein if the lesion is placed there, it
will explain all the signs and symptoms of the
patient.
LEVELS of LOCALIZATION
Meninges/CSF
Brain

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Supratentorial
cerebral hemispheres
basal ganglia
diencephalon
Infratentorial
brainstem (midbrain, pons, medulla)
cerebellum
Spinal Cord
Cervical
Thoracic
Lumbar
Sacral
Roots
Cranial
Spinal
Nerves
Cranial
Spinal
Neuromuscular junction
Muscle
Diffuse vs. focal
Diffuse: involves both sides
Focal: involves a localized area
left or right
intra-axial/intramedullary vs. extraaxial/extramedullary
intra-axial within the brain parenchyma
intramedullary within the spinal cord
ABNORMAL CEREBRAL FUNCTION
The different cerebral function tests are able to elicit a
specific cognitive impairment. When present, they can point
to a specific region of the cerebrum because of the different
functions of the different regions.
Frontal lobes
Lack of initiative and spontaneity
Personality changes
Slight impairment of intelligence
Decomposition of gait and stance, primitive reflexes,
incontinence
Motor dysfunction contralateral
Brocas aphasia
Conjugate gaze paresis
Temporal lobes
Dominant
Wernickes aphasia
auditory agnosia
dysnomia or amnesic aphasia
Non-dominant
inability to judge spatial relationships in rare
cases
impairment in non-verbal tests
inability to recognize melodies and non-lexical
qualities of music
Either temporal lobe
auditory illusions and hallucinations
psychotic behavior
(contralateral) upper homonymous
quadrantanopia Meyers loop of the optic
radiations wound around the temporal horn of
the lateral ventricle
Bilateral disease
Korsakoffs amnesic defect
apathy and placidity
increase sexual activity

sham rage
cortical deafness Heschls gyrus but of both
lobes
loss of other unilateral functions
Parietal lobes
Either Side
cortical sensory syndrome and sensory
extinction
mild hemiparesis (variable), unilateral muscular
atrophy in children, hypotonia, poverty of
movement, hemiataxia (all seen only
occasionally)
homonymous hemianopsia or inferior
quadrantanopsia
Left or Right
Neglect of the opposite side of external space
(more with right or the non-dominant parietal
lobe)
Dominant
Disorders of language (especially alexia)
Gertsmann syndrome agraphia, acalculia, right
and left disorientation and finger agnosia
Tactile agnosia
Bilateral ideomotor and ideational apraxia
Non-Dominant
Visuospatial disorder
Topographic memory loss
Anosognosia, dressing and constructional
apraxia (more with non-dominant)
Confusion
Tendency to keep eyes closed
Bilateral
Visual spatial imperception, spatial
disorientation and complete or partial Balint
syndrome (optic apraxia)
Occipital lobes
Either Side
Contralateral (congruent) homonymous
hemianopsia
Elementary hallucinations
Left Side
Right homonymous hemianopsia
Alexia and color-naming defect
Visual object agnosia
Right Side
Left homonymous hemianopsia
Visual illusions and hallucinations
Loss of topographic memory and visual
orientation
Bilateral
Cortical blindness but pupils will be preserved
Anton syndrome visual anosognosia, denial of
cortical blindness
Loss of perception of color
Prosopagnosia (temporo-occipital)
Simultanagnosia (parieto-occipital)
Balint syndrome (parieto-occipital)
Paralysis of R face, arm and leg
APPLICATION
Example 1
Step 1 : Signs
Paralysis of R face, R arm, R leg
Step 2 : Neuroanatomic Correlates
Paralysis of the Right face (corticobulbar tract)

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L cerebral cortex L subcortical white matter

L internal capsule L cerebral peduncle
L midbrain L upper and midpons -- R lower
pons (facial nucleus) R facial nerve R N-M
junction R facial muscles
Paralysis of the Right arm (corticospinal tract)
L cerebral cortex L subcortical white matter
L internal capsule L peduncle L
midbrain L pons L medulla -- R cervical
cord R brachial plexus R peripheral nerves
to the arm N-M junction R arm muscles
Paralysis of Right leg (corticospinal tract)
L cerebral cortex L subcortical white matter
L internal capsule L cerebral peduncle
L midbrain L pons L medulla -- R cervical
cord R thoracic cord R L-S cord R L-S
plexus nerves N-M junction muscles
Step 3 : Intersection
Anywhere within L cerebral hemisphere to L
midpons
with aphasia: cerebral cortex
without cortical signs: internal capsule
with CN III palsy opposite the hemiparesis: L
midbrain (Webers syndrome)
Example 2
Step 1 : Signs
Paralysis of L face, R arm, R leg
Step 2 : Anatomic Correlates
Paralysis of Left face
R cerebral hemisphere R midbrain R
upper and mid-pons -- L lower pons (facial
nucleus) L facial nerve N-M junction
muscle
Paralysis of Right arm
L cerebral hemisphere L brainstem -- R
cervical cord brachial plexus nerves NM junction muscles
Paralysis of Right leg
L cerebral hemisphere L brainstem -- R
spinal cord L-S plexus nerves N-M
junction muscles
Step 3 : Where is the intersection?
L brainstem specifically, L lower pons
crossed hemiplegia

Figure 1. Cortibulbar tract (blue) crosses at different levels. It

synapses before specific cranial nuclei supplied. Corticobulbar
tract to CN VII crosses at the lower pons before it synapses
with the facial nucleus. Corticobulbar tract to CN XII crosses
at the medulla before it synapses with CN XII nucleus.
Corticospinal tract (red) which crosses at the pyramid or
lower medulla before going down to the arm or the leg.

Figure 2. Corticospinal tract to the upper limb.

Figure 3. Corticospinal tract to the lower limb.

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Figure 10. Contralateral hemianopsia with macular sparing.

Lession at the Right occipital pole (6 in Figure 4).
Optic tract is extra-axial or outside the brain few
lesions
Optic radiations are intra-axial or within the brain more
common to have lesions
Example 3.
Patient with fever, headache of 9 days duration,
papilledema, visual field confrontation: Left superior
quadrantanopia
Lesion: abscess in Right temporal lobe

Figure 4. Visual pathway. Type of lesion can determine which

part of the visual pathway is affected.

Figure 5. Monocular blindness . Lesion at Right optic nerve (1

in Figure 4)

Example 4.
Patient with acute onset of R homonymous hemianopsia;
blindness of right visual field. To consider:
L occipital lobe lesion
L parietal-temporal lobe lesion
To decide: Determine whether patient has hemiparesis
or not.
If hemiparesis is present, the lesion is at the parietal
lobe because it will also affect the motor fibers.
If hemiparesis is not present, the lesion is at the
occipital lobe.

Figure 6. Bitemporal hemianopsia. Lesion at optic chiasm (2 in

Figure 4)
Figure 11.

Figure 7. Contralateral homonymous hemianopsia. Lesion is

at Right optic tract (3 in Figure 4).

Figure 8. Contralateral superior quadrantanopia. Lesion of the

right optic radiations (fibers that are more broadly dispersed)
at Meyers loop which is wounding around the temporal horn
of the lateral ventricle (4 in Figure 4).

Figure 9. Contralateral inferior quadrantanopia. Lesion of the

right optic radiations at the inferior parietal l obe (5 in Figure
4).

Figure 12. Lateral spinothalamic tract for pain.

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Brown-Sequard Syndrome weakness on same side

and numbness on the opposite side; hemisection of
the cord
The absence of localizing signs is by itself localizing.
Meningitis
Encephalitis
Subarachnoid hemorrhage
Migraine/tension headache
Metabolic encephalopathy
Case 1.
A 58-yr old man was found in his bedroom unconscious. On
examination, there is no response to pain. Pupils are small
but reactive. EOMs are full by dolls eye maneuver. Babinski
is present bilaterally. RBS was 30 mg%. He r egained
consciousness after D50W infusion.

Figure 13. Dermatomal chart will help localize.

Figure 14. Corticospinal tract. Descending motor pathway

(red) which decussates in the medulla. Ascending sensory
pathway. Dorsal columns (blue) uncrossed in the spinal cord;
crosses at the cervical cord medullary junction which follows
the pathway of the corticospinal tract but in reverse.
Example 5.
Signs:
weakness of Right leg, loss of joint position sense
and vibration sense of Right leg and loss of pain and
temperature of Left leg
Anatomic Correlates
weakness of Right leg
Left cerebral hemisphere -- R medulla
cervical cords thoracic lumbosacral cord
loss of joint position sense and vibration sense of
Right leg
Right Leg lumbosacral thoracic cervical
--X Left medulla cerebral hemisphere
loss of pain and temperature of Left leg
Left leg lumbosacral cord -- Right thoracic
cervical brain
Intersection
Can be anywhere between Right cervical to thoracic
cord
Not cervical because the arms are not involved
So lesion is at right thoracic cord

Step 1 :
No pain perception, (+) Babinski, decreased glucose,
loss of consciousness, small pupils
Step 2 : Anatomic correlates
No Pain Perception: Afferent nerve fibres from pain
receptor spinal cord cerebellum medulla
pons midbrain thalamus somatosensory
cortex (lateral spinothalamic tract. See Fig 11)
Abnormal Babinski, bilateral : Motor strip (cereb ral
cortex) midbrain pons medulla [upper
motor n eurons to L4]
Small pupils lateral genicula te body superio r
colliculus aqueduct Edinger-Westphal nuclei
convergen ce centre CN III Ciliary ganglion
Sphincter Pupillae
Step 3 :
The lesion may be isolated in the midbrain (wh ere CN
III emerges).
Ischemia fro m microvascular diseases a ssocia ted
with diabetes mellitus may explain th e symp toms.
Case 2.
A 58-yr old man was found in his bedroom unconscious.
There is no response to pain. BP was 200/120. Pupils were
pinpoint but reactive. No EO Ms were elicited on dolls eye.
Ocular bobbing was noted. Babinski sign was present
bilaterally.
Step 1 :
No pain perception, pinpoint pupils, (-) dolls eye
reflex, ocular bobbing, (+) Babinski
Step 2 :
No pain perception: Affer ent nerve fibres from pain
receptor spinal cord cerebellum brainstem
thalamus somatosensory cortex (lateral
spinothalamic tra ct. See Fig 11)
Abnormal babinski, bilateral: Motor strip (cereb ral
cortex) midbrain pons medulla [upper
motor n eurons to L4]
Pinpoint pupils: lateral genicula te body superior
colliculus aqueduct Edinger-Westphal nuclei
convergen ce centre oculomotor nucleus CN III
Ciliary ganglion Sphincter Pupillae
Negative dolls eye reflex (oculocephalic reflex):
horizontal semicircular canals hair cells
vestibular ganglion cells medial vestibular nucleus
contrala teral abducens nuclear complex CN VI
oculomotor nucleus CN III medial rectus
mus.

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Step 3 : Intersection
The intersection is found at the midbrain, where CN
III emerges.
In contrast from the previous case (which may
involve small vessels), a larger vessel may have b een
affected (e.g., posterio r cerebral artery).
Case 3.
A 53-yr old doctor was noted to have facial asymmetry while
on-duty at the ER in a community hospital. BP was 180/100.
On examination, the R eyebrow does not elevate well. There
is weak closure of the R eye. The L angle of the mouth is
pulled to the left on smiling. The rest of the N.E. was normal.
Step 1 :
Facial asymmetry (R eyebrow does not elevate well,
weak closure of R eye, L angle of mouth is pulled to
the left on smiling)

Incongruous homonymous hemianopsias are more

likely caused by optic tract lesions, while a mo re
congruous hemianopsia is more likely caused by
an occipital lobe defect.
<end of lectur e>

Book / Internet Sources

Harrisons Principles of Internal Medicine, 17th ed. (Vol
II, p. 2484: Approach to the Patient with Neurologic
Disease)
Manter and Gatzs Essentials of Clinical Neuroanatomy
and Neurophysiology, 10th ed.
DeMyers Technique of the Neurologic Examination, 5th
ed.
Pattens Neurological Differential Diagnosis, 2nd ed.
Neurowiki <http://wiki.cns.org>
Adams & Victor's Principles of Neurology (8th ed)
Disclaimer: We attempted to answer the cases ourselves. We
based our answers on the sources listed above but we could
have read them wrongly. Please approach any of us if youve
got questions, corrections, or complaints about this
transcription.

Step 2 :
Weak R eyebrow: Cerebral cortex Midbrain
upper pons Fibres fro m R & L co rticobulbar tracts
(50:50 innervation) R facial nucleus (at mid pons)
R facial nerve R fibres to muscle R muscle
Weak R orbicularis oculi: Cerebral cortex
midbrain Fibres from R & L corticobulbar tracts
(50:50 innervation) R facial nucleus R facial
nerve R fibres to muscle R orbicularis o culi
Pulled L mouth (overcompensation from paralyzed R
angle of mouth): Cerebral cortex Midbrain
upper pons Fibres fro m R & L co rti cobulbar tracts
(strongly from L side) R facial nucleus (at midpons) R facial nerve R fibres to muscle R
muscle
Step 3 : Intersection
The findings indicate a right-sided facial paralysis,
which indicates a lower moto r neuron (LMN) lesion.
An LMN lesion of CN VII may involve the facial
nucleus, the fascicle, or the main seventh nerve
trunk, leading to a loss of control of the ip silateral
facial muscles.
Case 4.
A 33-yr old female complained of progressive blurring of
vision on her left side for the past 4 months. On exam, ther e
was a left homonymous hemianopsia. Rest of neuro exam
was normal
Step 1 : progressive blurring, left homonymous
hemianopsia. No mention of light reflexes or pupil size.
Step 2 :
Left homonymous hemianopsia: R optic tract (see Fig
7) or left o ccipital striate co rtex
Step 3 :
Optic tract lesions can be caused by pituitary
tumours, craniopharyngiomas, chordomas, and
meningiomas. The o ccipital striate co rtex may be
affected by an infarction of the posterio r cerebral
artery.

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When I consider thy heavens, the work of thy fingers, the

moon and the stars, which thou hast ordained;
What is man, that thou art mindful of him? and the son of
man, that thou visitest him?
- Psalm 8:3-4

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