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Cortical Localization
David Roman Renner, MD
Department
of Neurology Reading
Resources:
Lindsay KW, Bone I, Callander R. Clinical
Presentation, Anatomical Conceps and Diagnostic Approach:
Higher Cortical Dysfunction. In:
Neurology and Neurosurgery Illustrated.
Philadelphia, Churchill Livingstone 1998, pp. 105-114.
Rolak LA. Approach to the Patient with Neurologic Disease.
In: Neurology Secrets. Philadelphia,
Hanley & Belfus, Inc. 1993, pp. 37-44. What
you are responsible for:
I will write all test questions for this lecture hour, the content of
which is addressed in this handout and/or the lecture hour.
Your test questions will only be derived from the section on cortical localization. The
remaining text is included to assist you in localizing lesions in the
neuraxis through a complete neurologic examination. Syllabus Contents:
Divisions of the Neuroaxis
Content of the Neurologic Examination
Clinical Hallmark of Lesions within the Neuraxis
Typical Neurologic Examination when Lesioning Various Levels of the
Neuraxis
Objectives: The student should be able to: 1.
state
how hemispheric dominance is defined 2.
lateralize
hemispheric dominance based upon language and handedness 3.
localize
lesions within the hemispheric cortex via clinical exam findings
(You will not be tested on information following the cortical
localization section.)
Localization
is important
Investigation modalities differ widely depending upon the level
affected Divisions of the Neuraxis: Cortical Brain Subcortical
Brain Brainstem Cerebellum Spinal
Cord Root Peripheral Nerve Neuromuscular Junction Muscle The neurologic exam allows one to accurately identify which segment of the neuraxis is lesioned. A complete neurologic exam varies between neurologists, but generally consists of testing of:
Higher cortical function
Cranial nerves
Cerebellar
Motor
Sensory
Reflexes
Gait and Station Higher Cortical Function: Depends upon hemispheric
dominance Non-neurologists are able to
state generalizations about hemispheric dominance: right:
visual/spatial, perception and memory left:
language and language dependent memory One should be able to further
localize lesions Cortical Brain:
Frontal Lobe: Left
sided lesions:
language Broca’s
Aphasia Right
sided lesions:
?judgement? Bilateral
lesions: precentral
gyrus: motor homunculous supplementary
motor cortex: eye and head turn prefrontal
cortex: personality, initiative paracentral
lobule: cortical inhibition of
voiding B/B Parietal
Lobe: Right
sided lesions: anosognosia:
left hemineglect dressing
and constructional apraxia geographic
agnosia Left
sided lesions: Gerstman’s Tetrad (not
triad): L/R confusion, finger
agnosia, acalculia, agraphia without alexia Bilateral
lesions:
Somatosensory homunculous abnormal
posture and passive movement localization
of touch 2-point
discrimination astereognosis Temporal: Right
sided lesions: hearing
language Left
sided lesions: hearing
sounds, rhythm, music Wernicke’s
Aphasia Bilateral
lesions: learning
and memory: mid/inferior gyri olfaction:
limbic Auditory
cortex: Heschel’s gyrus Occipital
Lobe: Right
sided lesions: micropsia macropsia
Left sided lesions:
? Bilateral
lesions: visual
hallucinations: elemental and
unformed prosopagnosia:
familiar faces cortical
blindness: striate cortices,
normal pupil rx Anton’s
syndrome: (para)striate, denial
of obvious blindness Balint’s
syndrome: inability to direct
voluntary gaze with visual agnosia Neurologic Examination when Cortical Brain is
Lesioned
Higher Cortical Function:
you may see an aphasia, apraxia, or an agnosia Cranial Nerves should be
normal, unless there is forced eye deviation Cerebellar function should be
normal Motor exam may reveal weakness
of face/arm>leg (or vice versa) with hypertonia
if corticospinal tracts are hit Sensory exam may be abnormal
(face/arm>leg, or vice versa) Reflexes may be abnormal
(hyper-reflexia), and Babinski’s reflex may
be present if the corticospinal tracts are hit Subcortical
Brain
Contains deep white radiating
fibers tightly packed together When lesioned, there is equal
involvement of face/arm/leg. Symptoms
can include
weakness or sensory abnormalities Visual abnormalities
occur due to interruption of radiating fibers are contained within
the subcortical brain deep
parietal: bilateral homonomous
quad on the floor deep
temporal (Meyer’s loop): bilateral
homonomous quad in the sky Neurologic Examination when
Subcortical Brain is Lesioned Higher cortical function should
be normal Cranial nerves may reveal a
visual field cut Cerebellar function is usually
normal Motor exam may reveal weakness
in face=arm=leg with hypertonia Sensory exam may reveal sensory
abnormalities in face=arm=leg Reflexes may be abnormal
(hyper-reflexia) with increased tone, and Babinski’s
reflex may be present if corticospinal tracts are lesioned Brainstem
The brainstem is basically a
spinal cord with embedded cranial nerves Cranial nerve symptoms
with long tract symptoms characterize brainstem disease Long
Tract signs: (bilateral and
crossed) corticospinal
(pyramidal): motor spinothalamic:
pain/temp to the thalamus dorsal
columns: prioprioception/vibration
to thal. (due
to decusation of long tracts, BS lesions do not produce horizontal motor/sensory
levels as in the cord, but rather vertical levels of hemiparesis/hemidysesthesias) Neurologic
Examination when Brainstem is Lesioned
Higher cortical function should
be normal Cranial nerves may be abnormal III,
IV, VI: diplopia V:
decreased facial sensation VII:
drooping VIII:
deaf and dizzy IX,
X, XII: dysarthria and dysphagia XI:
decreased strength in neck and shoulders Cerebellar Function should be
normal Motor exam may reveal
hemi-paresis and hemi-hypertonia Sensory exam may reveal sensory
abnormalities Reflexes may be abnormal
(hyper-reflexia) including the jaw jerk reflex,
with increased tone, and Babinski’s reflex Cerebellar Function
Some people believe that one
can not test specifically for cerebellar abnormalities no
single test on examination reliably evaluates the cerebellum H: hypotonia A: assynergy of (ant)agonist muscles N: nystagmus D: dysmetria, dysarthria S: stance and gait T: tremor Neurologic
Examination when the Cerebellum is Lesioned Higher cortical function should
be normal Cranial nerves should be normal Cerebellar function may reveal
nystagmus, flaccid dysarthria Motor exam should show
preserved strength, with ipsilateral hypotonia, an ataxic tremor,
dysmetria Sensory exam should be normal Reflexes should be normal Spinal
Cord
Sensory level Spasticity/hypertonia almost
always in the legs, sometimes in the arms if the lesion
is high enough Weakness
in the legs, extensors > than flexors, distal > proximal Bowel and bladder
involvement producing incontinence Neurologic Examination when the Spinal Cord is
Lesioned
Higher cortical function should
be normal Cranial nerves should be normal Cerebellar function should be
normal Motor exam reveals bilateral
leg weakness (extensors worse than flexors) below the
lesion with increased tone/spasticity Sensory exam reveals a sensory
level which may be assymetric Reflexes are increased (hyper-reflexic)
below the level (clonus?) With
Babinski’s reflex, and the loss of superficial reflexes (Beavor’s sign, cremasteric,
anal wink, etc) Root/Radiculopathy
Pain
is the hallmark of a radiculopathy Sensory abnormalities should
localize to a dermatome provocative
maneuvres exacerbate the discomfort Asymmetric weakness in a
myotome proximal
(C5C6) distal
(L5S1) (because
the most common radiculopathy in the cervical region produces proximal weakness, and the most
common radiculopathy in the lumbosacral region produces distal weakness, one
cannot make the statement that radiculopathies “tend to produce
proximal/distal weakness.” Neurologic Examination when a Root is Lesioned
Higher cortical function should
be normal Cranial nerves should be normal Cerebellar function should be
normal Motor exam may reveal
assymetric weakness, atrophy, and fasiculations in a myotome Sensory exam may reveal
assymetric dysesthesias confined to a dermatome Reflexes may be decreased
(hypo- to a-reflexia if the root carries a reflex) Peripheral Nerve (nonfocal) Weakness that is distal
predominant, which may start a bit asymmetric, but with time,
looks symmetric Sensory
dysesthesias that are distal predominant Autonomic involvement may occur Difficulty
focusing eyes Erectile
dysfunction Dyshydrosis:
changes in the pattern of sweating Constipation Cardiac
arrhythmias Trophic changes:
smooth shiny skin, vasomotor abnormalities (edema, temperature
dysregulation, vascular flushing), hair loss, nail changes Neurologic
Examination with Diffuse Peripheral Nerve Lesioning
Higher cortical function should
be normal Cranial nerves should be normal Cerebellar function should be
normal Motor exam may reveal
distal-predominant weakness, atrophy, and fasiculations Sensory exam may reveal
distal-predominant sensory loss Reflexes may reveal distal
hypo- to a-reflexia Neuromuscular
Junction
Fatiguability
is the hallmark Weakness:
proximal and symmetric exacerbated
with use, recovers with rest often
affects facial muscles (ptosis, dysconjugate gaze, slack jaw) muscles
have normal bulk and tone Sensation:
preserved Neurologic Examination in Disorders of the
Neuromuscular Junction
Higher cortical function should
be normal Cranial nerves may show
fatiguable ptosis, dysconjugate gaze, slack jaw Cerebellar function should be
normal Motor exam may reveal
fatiguable proximal weakness in both UE’s and LE’s no
atrophy or fasiculations tone
may be slightly decreased Sensory exam should be normal Deep tendon reflexes may be
hypo- to a-reflexic in Lambert Eaton Myasthenic Syndrome,
or normal in MG Muscle
Symmetric proximal weakness
of arm and leg muscles Sensation is normal (though
patients complain of cramping and aching) Neurologic Examination in Disorders of Muscle
Higher cortical function should
be normal Cranial nerves may reveal nonfatiguable
ptosis, dysconjugate gaze, slack jaw, dysphagia,
dysphonia, (dysarthria) Cerebellar function should be
normal Motor exam reveals symmetric
proximal weakness in both UE’s and LE’s atrophy
and fasiculations Sensory exam should be normal Reflexes should be preserved
until late in the disease
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Last updated: 10/05/2002 © 2000-2002 John Rose, MD University of Utah School of Medicine |
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