Exam
Neurologic Lesion Localization
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Neurologic Lesion Localization
, Localization of Neurologic Deficit
See Also
Neurologic Exam
Causes
Peripheral Nerve
See
Peripheral Neuropathy
Dermatome
Distribution of sensory changes
Pain in
Dermatomal Distribution
suggests peripheral cause
Contrast with higher lesions which follow non-dermatomal loss of
Sensation
Lower Motor Neuron Lesion
(LMN)
LMN findings include
Flaccid Paralysis
, muscular atrophy,
Fasciculation
s and hyporeflexia
Contrast with
Upper Motor Neuron Lesion
s (UMN) with overall
Muscle
group weakness, spasticity and hyperreflexia
Causes
Spinal Cord
See
Spinal Cord Syndrome
Difference in
Sensation
loss may identify lesion level
Pain and
Temperature
sense (
Spinothalamic Tract
) crosses to contralateral side within 1-2 levels
Conscious proprioception (
Posterior Column
s) crosses to contralateral side at the
Medulla
Unconscious proprioception (
Spinocerebellar Tract
) never crosses (remains ipsilateral)
Causes
Brainstem
See
Brainstem
Cranial Nerve
deficits indicate lesions in the peripheral
Cranial Nerve
, the
Brainstem
or above
Multiple
Cranial Nerve
deficits suggest a
Brainstem
lesion (see
Cranial Nerve Nucleus
)
Peripheral
Cranial Nerve
deficit may also cause this (e.g.
Cavernous Sinus
contains
CN 3
,
CN 4
,
CN 5
,
CN 6
)
Bilateral
Cerebral Hemisphere
or
Internal Capsule
lesions may also cause multiple
Cranial Nerve
deficits
Cranial Nerve
lesions contralateral to extremity deficits suggests a
Brainstem
lesion
Lesion must be above the spinal cord to affect
Cranial Nerve
s
Cerebral Hemisphere
lesions will affect the same contralateral side for both
Cranial Nerve
and extremity
Extremity motor and sensory central innervation crosses in the
Medulla
Cranial Nerve
central innervation crosses above their nucleus level
Causes
Cerebellum
See
Cerebellum
See
Cerebellar Function Test
Incoordinated INTENTIONAL movement
Ataxia
See
Acute Cerebellar Ataxia
See
Cerebellar Gait
Altered
Posture
and gait
Patient falls on the same side as a
CNS Lesion
Incoordinated movement
Dysmetria (overshooting on
Finger-Nose-Finger Test
)
Dysdiadochokinesia
(difficult
Rapid Alternating Movements
)
Scanning speech (irregularly spaced sounds, words, phrases)
Tremor
See
Cerebellar Tremor
Intention Tremor
(during purposeful movement)
Nystagmus
Causes
Basal Ganglia
See
Basal Ganglia
See
Movement Disorder
Incoordinated UNINTENTIONAL movement
Parkinsonism
(
Basal Ganglia
and
Substantia Nigra
degeneration)
Associated with rigid slow movements, resting
Tremor
, shuffling gait, mask-like facies
Athetosis
Slow, writhing movements (esp. hand, wrist)
Chorea
(e.g.
Huntington's Chorea
,
Sydenham's Chorea
)
Sudden, jerky movements
Hemiballismus
Sudden, incoordinated flailing of an extremity
Causes
Cerebral Hemisphere
s -
Frontal Lobe
See
Frontal Lobe
Hemiparesis
(
Brodmann Area 4
) with or without spasticity and hyperreflexia (
Brodmann Area 6
)
Gait
disturbance
Generalized Seizure
s or
Focal Seizure
s
Expressive Aphasia
(
Brodmann Area 4
4, 45)
Behavior and Personality change (lesions anterior to the
Primary Motor Area
,
Brodmann Area 4
)
Judgment and abstract thinking affected
Affects
Instrumental Activities of Daily Living
May present with concerns for
Dementia
Causes
Cerebral Hemisphere
s -
Parietal Lobe
See
Parietal Lobe
Receptive Aphasia
(
Brodmann Area 39
)
Sensory loss (
Brodmann Area
3,1,2 and Area S2 following
Homunculus
distribution)
Spatial
Disorientation
(
Brodmann Area 5
, 7)
Hemianopia
(loss of half of
Visual Field
in each eye)
Agnosia
of tactile
Sensation
and proprioception (
Brodmann Area 40
, dominant hemisphere)
Apraxia
(difficulty with skilled movement) and altered left-right discrimination (
Brodmann Area 40
)
Causes
Cerebral Hemisphere
s -
Temporal Lobe
See
Temporal Lobe
Complex Partial Seizure
s or
Generalized Seizure
s
Quadrantanopia
(
Vision Loss
or anopia in a
Visual Field
quadrant)
Behavioral alterations
Memory Loss
(esp. visual memories)
Receptive Aphasia
(dominant hemisphere,
Brodmann Area 22
)
Causes
Cerebral Hemisphere
s -
Occipital Lobe
See
Occipital Lobe
Contralateral
Hemianopia
References
Goldberg (2014) Clinical Physiology, Medmaster, Miami, p. 108
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