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Neuro Lesions

Neuro Lesions

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Published by kep1313
medical school neuroscience
medical school neuroscience

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Published by: kep1313 on Mar 24, 2013
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Neuro: Lesions
PRINCIPLES
 
SPINAL CORD LESIONS:
Can be contralateral, ipsilateral, or bilateral. See figure below.
 
o
 
Total transection
Loss of ALL sensation and motor controlbilaterallyat all levels below the lesion.
 
o
 
Loss of central portion
Loss of ALL sensation and motor controlbilaterallyat every level below the lesion EXCEPT the sacral dermatomes(sacral sparing).
 
o
 
Hemisection
Loss of fine touch/propriocep/vibration (DC/ML)ipsilaterallyLoss of crude touch/pain/temp (STT)contralaterallyat all levels below the lesion.
 
o
 
Loss of white commissure
Loss of crude touch, pain, and temp (STT)bilaterallyat the level of the lesion but NOT below the lesion.
 
o
 
Loss of dorsal columns
Loss of fine touch, proprioception and vibration (DC/ML) bilaterally
 
o
 
Loss of anterolateral system
Loss of 
 
crude touch, pain, and temp (STT)bilaterally
 
o
 
Loss of spinocerebellar tracts
Ataxia
 
 
BRAIN STEM LESIONS:
Can be contralateral or ipsilateral.
 
o
 
Medial Lesions
Loss of contralateral
 
motor control
 
(pyramidal tracts).
 
o
 
Lateral Lesions
Loss of crude touch, pain, and temp (TTT) inipsilateralface
 
Loss of fine touch, proprioception, and vibration (DC/ML) incontralateralhalf of entire body  This occurs because the spinothalamic and spinal trigeminal tracts are
adjacent 
in the lateral part of the brainstem.
o
 
Vertebrobasiliar Stroke Lesions
Three Ds: Contralateral Dysarthria (DC/ML), Ipsilateral Diplopia (CN6), Ipsilateral Dysphagia (CN9 & 10)
 
 
CEREBRAL LESIONS:
Always contralateral.
 
o
 
Internal Capsule Lesion
 Loss of ALL sensation and motor controloncontralateralhalf of body(pyramidal and thalamic somatosensory tracts) Muscle weakness onlower quarterof face(corticobulbar tracts) Ventral lesions present withcontralateral homonymous hemianopsiaIN ADDITION to these sx if optic radiations are affected
 
CEREBELLAR LESIONS
 
o
 
Vermis
Trunk ataxia, abnormal eye movements (diplopia)
o
 
Hemispheres
Ipsilateral limb ataxia, intention tremor, fall toward the side of the lesion
 
UMN vs. LMN LESIONS:
Everything is
lowered 
in LMN lesion and
ramped up
in UMN lesions. Note that fasciculations occur with LMN lesions, NOT UMN!
 
CENTRAL NERVOUS SYSTEM
 – 
CEREBRUM
 Aphasia, Agnosia, Apraxia
 
Location of Lesion Name of Disease Disease Mechanism Effects
(Relative to Location of Lesion)
 Non-dominant Parietal LobeSPATIAL NEGLECTSYNDROMECognition:
 Agnosia of the
contralateral
 side of the world.
Broca’s area
 
BROCA’S APHASIA
 
Stroke in
MCA
.
Cognition:
Influent speech with intact understanding.
 
Broca’s area
 
WERNICKE’S
APHASIA
Stroke in
MCA
.
Cognition:
Fluent speech with impaired understanding.
 Thalamus, Caudate, Occipital Lobe
WEBER’S SYNDROME
 
Stroke in
PCA
.
Contralateral Body:
 Loss of pain and temperature sensation due to loss of STT,deficits of CN7, CN9 & CN10, hemiparesis and UMN lesion sx, Parkinsonism dueto loss of substantia nigra
Contralateral Face:
Lower face weakness due to loss of corticobulbar tract.
Contralateral Eye:
 Contralateral hemianopia with macular sparing,
Ipsilateral Eye:
 
Horner’s syndrome due to
CN3 deficit (ptosis, fixed pupil, down& out gaze).
 
 
CENTRAL NERVOUS SYSTEM
 – 
CEREBELLUM, LIMBIC SYSTEM, DIENCEPHALON, BASAL GANGLIA
Location of Lesion Name of Disease Disease Mechanism Effects
(Relative to Location of Lesion)
 CEREBELLUM
 Ataxia
VermisAxial Muscles:
 Truncal ataxia, dysarthria.
HemisphereAppendicular Muscles:
 Body falls
toward 
 
ipsilateral
 side.
Cerebellopontine AngleACOUSTIC NEURINOMA
Tumor spreads from inner ear tothe cerebellopontine angle,where CN7 and CN8 exit thebrainstem. Tumor compressesCN7 & CN8. Can also compressCN9, CN10 and corticospinaltracts.
Ipsilateral Ear:
Dizziness, pulsating tinnitus
deafness.Loss of higherfrequencies first. Contrast with
Mieniere’s disease, which loses lower
frequencies first. 
Ipsilateral Face:
 Paralysis of facial muscles and loss of corneal reflex(efferent arm) due to loss of CN7.
Ipsilateral Body:
 Ataxia due to loss of CN8 and corticospinal tracts.
Throat:
 Hoarseness and trouble swallowing due to loss of CN9 & 10.
Tongue
: Loss of taste due to loss of CN7.
LIMBIC SYSTEM
 Anterograde Amnesia &InappropriateBehavior 
Amygdala
(Bilat)
 KLUVER-BUCY SYNDROME
Associated with HSV-1.
Behavior:
 Hyperorality, hypersexuality, disinhibited behavior.
HippocampusANTEROGRADE AMNESIAMemory:
 Unable to make NEW memories. Old memories are intact.
DIENCEPHALON
Vegetative States &EndocrineImbalance
Mammillary Bodies
(Bilat)
 WERNICKE-KORSAKOFFSYNDROMECognition:
 Confusion, ophthalmoplegia, ataxia with memory loss,confabulation, personality changes.
Reticular Activating SystemCOMAArousal:
Reduced arousal and wakefulness.
BASAL GANGLIA
Dyskinesia
Subthalamic NucleusHEMIBALLISMUS
Disinhibition of basal gangliaoutput.
Contralateral Limb:
 Wild, flailing involuntary movements.
Striatum
HUNTINGTON’S DISEASE
 
Disinhibition of basal gangliaoutput.
Chorea
(sudden, jerky, dancing movements),
athetosis
(slow, writing,snake-like movements), aggression, depression, dementia. Ofteninitially mistaken for substance abuse.
Substantia Nigra
PARKINSON’S DISEASE
 
Inhibition of basal gangliaoutput due to destruction of dopaminergic neurons.
Muscle rigidity
(cogwheel rigidity),
bradykinesia
,
resting tremor
(pill-rolling between thumb and index finger), expressionless face, stoopedposture,
shuffling gait
, postural instability,
dementia
.
** Chorea: Sudden, jerky, dancing movements of limbs.** Athetosis: Slow, writing, snake-like movements of fingers.** Myoclonus: Sudden, brief muscle contraction (jerk or hiccup).
** Dystonia: Sustained involuntary muscle contraction (writer’s cramp, blepharospasm).
 ** Tremor: Rhythmic contraction and relaxation of muscles in one or more body parts (most often the hands).

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