Transcript Motor System Lesions Apraxia/Dyspraxia

Neuroanatomy
and
Neurophysiology
Sensory
• Afferent
•
•
•
•
•
•
•
•
•
Vision
Kinesthesia
Olfaction
Hearing
Taste
Pain
Temperature
Touch
Balance
Motor
• Efferent
• Glands
• Muscle
• Organs
•
•
•
•
•
Circulation
Digestion
Respiration
Excretion
Reproduction
,Viscera
Dendrite
Cell Body
Axon
Boutons contain:
-neurotransmitters
for excitation or
inhibition of
response
-mitochondria
for energy
generation and
protein development
Presynaptic
neurons
Postsynaptic
neurons
Meningeal Lining
protective and nutritive
function
Cortex=Bark
6 layers of cells
Pyramidal
motor cells
Non Pyramidal
sensory cells
Broadman’s Map
1,2,3,4,6,8,17,18,22,
41,42,44,45
Fissure
Gyri
Sulci
Frontal Lobe
precentral gyrus
supplemental motor area
inf. frontal gyrus=
pars operculum=
Broca’s Area
Parietal Lobe
postcentral gyrus
supramarginal gyrus
angular gyrus
Temporal Lobe
superior temporal gyrus
Heschl’s Gyrus
Wernicke’s Area
Occipital Lobe
calcarine sulcus
Projection
to
and from cortex to
brain stem, spinal cord
– Corona Radiata
Myelinated
Fibers
Association
links regions of same
hemisphere
Short connect one
gyrus to the next
Long interconnect
lobes of the brain of
the same hemispherearcuate fasciculus
Commissural
from one location on
one hemisphere to the
corresponding
location in the other –
corpus callosum
Corona
Radiata
Subcortical
Structures
Control of background
movement
initiation of movement
patterns
Lesions
basal ganglia =
extrapyramydal
dysfunction including
hypokenetic and
hyperkenetic
dysarthria
Basal
Ganglia
Cerebrovascular
System
Carotid Division
ext&int carotid
Int. carotid =
Ant. Cerebral a.
Mid. Cerebral a.
Vertebral Division
ant&post spinal a.
basilar arteries =
sup/ant cerebellar a.
post cerebral a.
Cerebralvascular
Obstruction
• Thrombosis is a stationary obstruction
• Embolus is a traveling clot that obstructs
• Aneurysm is a dilation or ballooning of a vessel wall which can
cause a rupture into surrounding space
• Congenital, AVM
• Trauma
• CVA, TIA
Anatomy of the
Brainstem
II
Olfactory I
Reaches the
brain without
going through
thalamus
Olfactory cortex
in pyriform lobe
and hippocampal
formation
CN II Optic Nerve
CN III oculomotor
CN IV Trochlear
CN VI Abducens
CN V Trigeminal
Sensory/motor
3 branches
opthalmic:
transmits sensory
information from
skin of the upper
face
maxillary:
transmits sensory
information from the
middle face
mandibular: sen/mot sensory from lower face,
kinesthetic/proprioceptive sense of m. of mastication, sen.
ant. 2/3 of tongue & floor of mouth (pain/temp), motor
innervates m. of mastication, tensor tympani and veli palatini,
mylohyoid, ant. belly of digastric
UMN Damage:
increased jaw
jerk reflex
LMN Damage:
atrophy/weakne
ss of affected
side,
jaw
pulls to
unaffected side
on closure
bilateral-jaw
hangs open
TVP damage:
hypernasality
Efferent for facial m.
Afferent: -taste ant. 2/3 tongue
-sublingual/submandibular
glands
UMN damage: no upper face paralysis
LMN damage: upper/lower face
paralysis on side of lesion
VII CN S/M
Facial
Upper face innervated
bilaterally
Lower face contralateral
VIII CN S/M
Vestibulocochlear
IX CN
S/M
Glossopharyngeal
Part of Pharyngeal
Plexus
Efferent
stylopharyngeus
Afferent
taste posterior 1/3
tongue, soft palate
Pain, temp., touch
posterior 1/3
X CN
Vagus S/M
Pharyngeal, superior,
and laryngeal branches
important in voice,
speech, and swallowing
Lesions can cause:
Lack of sensation in
pharynx
Lack of muscle function:
palate, pharynx, vocal
fold, esophagus
Large autonomic role
IX CN
Accessory M
Part of pharyngeal
plexus for innervation
of larynx, pharynx, and
soft palate
Sole innervation for
trapezius and SCM
XII CN
Hypoglossal M
Innervation for the motor function of the tongue
Each hypoglossal nucleus served by contralateral
corticobulbar tract
(L) UMN damage = (R) tongue weakness
(L) LMN damage = (L) tongue weakness
Fibers of the Corticobulbar Tract decussate prior to
reaching the hypoglossal nucleus, therefore
(L)
UMN damage/ (R) LMN damage = (R) tongue weakness
Dorsal Root +
Ventral Root =
Spinal Nerve =
Dorsal & Ventral
Rami
Branches of
ventral rami go to
sympathetic
ganglia, nuclei of
ANS
Efferent neurons
of dorsal and
ventral rami go to
motor end
plates/muscle
synapse
Spinal Reflex Arc
UMN: commands from
upper brain levels that
activate or inhibit
muscle function by
synapsing with LMN
LMN: dendrites and
soma within the spinal
cord,axons/components
that communicate with
muscle fiber
Neuron within ventral
gray matter is LMN or
Final Common Pathway
UMN/LMN
• LMN Damage: muscle weakness or complete paralysis,
reflexes not intact
• UMN Damage: muscle weakness or complete paralysis,
reflexes intact because a spinal arc reflex is a LMN process
AST Tract: transmits
info. On sense of light
touch from spine to
thalamus
Ipsilateral:
sensations on the
same side as they
enter the cord
Contralateral:
sensations on the
opposite side as they
enter the cord
Decussate:
cross the midline
Corticospinal
Tract
Pyramidal Tract
Voluntary
Movement
Modification of
Reflexes
Visceral Activation
Two neuron pathway
consisting of an UMN
and LMN
Corticobulbar
Tract
Arises from:
cortical cells in lateral
aspects of pre central
gyrus
premotor/somesthetic
regions of parietal lobe
Axons will:
branch/decussate at
different levels of
brainstem
synapse with nuclei of CN
Sensory Information:
facilitate/inhibit
transmission to thalamus
Serves:
CN for speech
Higher Functioning
• Primary activity areas: receive information from senses,
extract info.
• Adjacent higher order areas of processing (secondary,
tertiary,quaterary): info. compared to other info. received
and stored associated with modality
• Association areas: highest level of cognitive processing
Motor Function
• Identify target: tongue tip to alveolar ridge
• Spacial orientation: integration of information of body parts in
space
• Posterior parietal lobe receives information from thalamus,
cerebellum, basal ganglia
• Develop plan to achieve target behavior
• Premotor region, area 6, anterior to motor strip plans the action,
receives info from areas 1,2,3 re location of muscles and joints
• SMA, area 6 sup. & med., preparatory speech act, initiation of
speech act
• Execute plan: muscle movement with accurate timing
force and rate
• Area 4 execution of voluntary movement
Motor System Lesions
• Dysarthria: speech disorder arising from paralysis, muscular weakness,
and dyscoordination of speech musculature
• Flaccid Dysarthria: LMN damage of CN,
dysphonia due to VF paralysis, fasciculations,
hypotonia, reflexive responses reduced or absent
• Spastic Dysarthria: UMN bilateral damage to
pyramidal or extrapyramidal tracts, hyperreflexia, hypertonia
• UUMN: less devastating than bilateral
Motor System Lesions
• Ataxic Dysarthria: Damage to the cerebellum &/or brainstem
vestibular nuclei
• Loss of coordination, unable to achieve articulatory target,
problems in coordination of rate, range, and movement
• Dysdiadochokinesia
• Dysprosody
Motor System Lesions
• Hypokenetic Dysarthria: paucity of movement, inhibited initiation of
movement, reduced ROM, rigidity, pill rolling hand tremor
• Damage to BG &/or substantia nigra (SN)
• SN produces Dopamine (DA) which balances
acetylcholine (Ach), decreased DA results in inhibited
initiation of motor function
• Speech rushed, reduced duration of speech sounds, monopitch, monoloudness
Motor System Lesions
• Hyperkenetic Dysarthria:Extraneous involuntary movement caused by BG
circuit damage
• Subthalamic N. damage: inhibition to GP is lost resulting in Ballism (uncontrolled
flailing)
• BG damage: if Ach is decreased and DA increased choreiform, involuntary
twitching and movements, result
• Tics: rapid movements of small groups of muscle fibers
• Tremors: rhythmic contractions
• Athetosis: slow, writhing movements
• Dystonia: involuntary movement to a posture, posture held briefly
Motor System Lesions
• Mixed Dysarthria: Damage to more than one
of the controlling systems
• S/F: found in ALS, disease of UMN & LMN
• S/A: found in MS, UMN and cerebellum
• S/A/hypo: Wilson’s disease (hepatolenticular
degeneration)
Motor System Lesions
• Apraxia/Dyspraxia: A dysfunction of motor planning in the absence of
muscular weakness or dysfunction
• SMA damage: difficulty in initiating speech
• Dominant insular cortex damage: verbal dyspraxia (loss of fluency and groping
behavior, ability to contract musculature voluntarily is impaired)
• Oral apraxia: inability to perform non speech oral gestures
• Supramarginal Gyrus damage: verbal apraxia affecting long and complex
sentences
Hemispheric Specialization
• Left Hemisphere
•
•
•
•
Lateral Fissure is longer
Planum Temporale (HG) is larger
Generally functional dominance for L/S
Processes consonant transitions and stop consonant
bursts in (R) handed
• Process of analysis, favored discrete, sequential, brief
duration or rapidly changing information
• Spoken/written language perception & production
Hemispheric Specialization
• Right Hemisphere
• Spatial and holistic elements
• Face recognition
• Speech intonation
• Melody, tonal information
• Perception of form
• Intention of speaker
Lesion Studies
• Speech and Language Areas
• Wernicke’s Area (22): receptive or fluent aphasia
•
•
•
•
•
•
Relatively normal flow of speech
Has syntax
Does not understand what is said
Verbal paraphasias (substitution of words)
Neologisms (new word), jargon, word salad
Cannot repeat
Lesion Studies
• Broca’s Aphasia: lesions to 44,45, operculum of frontalparietal, insula, supramarginal gyrus of parietal lobe
•
•
•
•
Difficulty with the planning of speech
Non fluent aphasia
Expressive abilities severely limited
Usually retain auditory and visual input
Lesion Studies
• Global Aphasia: Damage to both Wernicke’s and Broca’s Area
and some sub cortical structures
• Both receptive and expressive functions are severely impaired
Lesion Studies
• Conduction Aphasia: lesion of arcuate fasiculus connecting Broca’s and
Wernicke’s area
• problem with repetition of words
• Anomia: difficulty naming objects
• Thalamic damage, cortical and subcortical structures
Lesion Studies
• Dyspraxia: : inability to program the articulators for
voluntary speech and non speech movements
• Frontal lobe insular cortex damage: difficulty producing simple
gestures with articulators (executive dyspraxia)
• Supramarginal gyrus damage: difficulty sequencing more
complex articulatory gestures ( planning dyspraxia)
Lesion Studies
• TBI/Right Hemisphere Damage
•
•
•
•
•
•
•
•
•
•
Decision making
Problem solving
Judgment
Response inhibition
Pragmatics
Emotional lability
Personality characteristics
Communication of emotion, intent, humor
Abstract information
Frontal- response inhibition
Lesion Studies
• Parahippocampal region
• Learning complex tasks
• Remembering information received through sensory
modalities
• Hippocampus
• Bilateral produce profound short term memory
deficit
• Unilateral produce milder deficit
• Removal of (L) difficulty remembering verbal
information