Transcript The Sensorimotor System

Sensorimotor systems
Learning, memory & amnesia
Chapters 8 and 11
Three principles of sensorimotor
function

hierarchical organization


Two other organizing characteristics?
motor output is guided by sensory input
The case of G.O. – darts champion
 The exception?


learning changes the nature and locus of
sensorimotor control
Posterior Parietal Association Cortex
Function: Integrates of sensory information
to plan and initiate voluntary movement
and attention.
Sensory system inputs: visual, auditory and
somatosensory.
Outputs: dorsolateral PFC, secondary motor
cortex and frontal eye fields.
Dorsolateral PFC
Frontal eye
field
Auditory
cortex
Visual
cortex
Inputs to Posterior Parietal
Association Cortex
Dorsolateral PFC
Frontal eye
field
Auditory
cortex
Visual
cortex
Outputs to Posterior Parietal
Association Cortex
Damage to the Posterior Parietal
Association Cortex
Can produce a variety of deficits
 Attention
 Perception and memory of spatial
relationships
 Reaching and grasping
 Control of eye movements
Damage to the Posterior Parietal
Association Cortex
Apraxia – a disorder of voluntary movement
not attributable to a simple motor deficit
(weakness or paralysis) or to a deficit in
comprehension or motivation.
Results from unilateral damage to the left
posterior parietal cortex.
Damage to the Posterior Parietal
Association Cortex
Contralateral neglect – a disturbance in a
patient’s ability to respond to stimuli on the
side of the body contralateral to a brain
lesion (not a simple sensory or motor
deficit).
Often associated with large lesions of the
right posterior parietal lobe.
Dorsolateral Prefrontal Cortex
Function: plays a role in the evaluation of
external stimuli and initiation of voluntary
responses to those stimuli.
Main input: posterior parietal cortex
Outputs: secondary motor cortex
primary motor cortex
frontal eye fields
Dorsolateral Prefrontal connectivity
Dorsolateral Prefrontal cortex
Neurons in this area respond to the
characteristics of objects (e.g.,
color/shape), the location of objects or to
both.
The activity of other neurons is related to the
response itself.
Secondary motor cortex
Input: most from association cortex
Output: primary motor cortex
Two classic areas:
1) SMA
2) Premotor cortex
Secondary Motor Cortex
Current classifications suggest
 At least 7 different areas
 3 supplementary motor areas
SMA and preSMA and
Supplementary eye field
2
premotor areas
PMd and PMv
 3 cingulate motor areas
 CMAr,
CMAv and CMAd
Secondary Motor Cortex
Subject of ongoing research
 In general, may be involved in
programming patterns of movements
based on input from PFC
 Mirror neurons – in premotor cortex (also
in posterior parietal cortex) are involved in
social cognition, theory of mind and may
contribute to autism if dysfunctional.

Primary Motor Cortex




Precentral gyrus of the frontal lobe
Major point of convergence of cortical
sensorimotor signals
Major point of departure of signals from cortex
Somatotopic – more cortex devoted to body
parts which make many movements
Motor
homunculus
Primary Motor Cortex

Monkeys have two hand areas in each
hemisphere, one receives feedback from
receptors in skin.

Stereognosis – recognizing by touch – requires
interplay of sensory and motor systems

Damage to primary motor cortex



Movement of independent body parts (e.g., 1 finger)
Astereognosia
Speed. accuracy and force of movement
Other sensorimotor structures
outside of the hierarchy
(sometimes called extrapyramidal systems)
 Cerebellum
 Basal ganglia
both modulate and coordinate the activity of
the pyramidal systems by interacting with
different levels of the hierarchy.
Cerebellum


10% of brain mass, > 50% of its neurons
Converging signals from



primary and secondary motor cortex
brain stem motor nuclei (descending motor signals)
Somatosensory and vestibular systems (motor
feedback)

Involved in motor learning, particularly
sequences of movement

Damage to cerebellum – disrupts direction, force,
velocity and amplitude of movements; causes tremor
and disturbances of balance, gait, speech, eye
movement and motor sequence learning .
Basal Ganglia
A collection of nuclei
 Part of neural loops that receive cortical
input and send output back via the
thalamus (cortical-basal ganglia-thalamocortical loops)
 Modulate motor output and cognitive
functions
 Cognitive functions of the basal ganglia

Descending Motor Pathways

Two dorsolateral



Two ventromedial



Corticospinal
Corticorubrospinal
Corticospinal
Cortico-brainstem-spinal tract
The corticospinal tracts are direct pathways
Dorsolateral Vs Ventromedial
Motor Pathways
Dorsolateral
 one direct tract, one
that synapses in the
brain stem
 Terminate in one
contralateral spinal
segment
 Distal muscles
 Limb movements
Ventromedial
 one direct tract, one
that synapses in the
brain stem
 More diffuse
 Bilateral innervation
 Proximal muscles
 Posture and whole
body movement
Experiments by Lawrence and
Kuypers (1968)
Experiment 1: bilateral transection of the
Dorsolateral (DL) corticospinal tract
Results:
1) monkeys could stand, walk and climb
2) difficulty reaching but improved over time
3) could not move fingers independently of
each other or release objects from their
grasp.
Experiments by Lawrence and
Kuypers (1968)
Experiment 2:
The same monkeys with DL corticospinal tract
lesions received 1 of 2 additional lesions:
1) The other indirect DL tract was transected
2) Both ventromedial (VM) tracts were
transected
Experiments by Lawrence and
Kuypers (1968)
Experiment 2 Results:
• The DL group could stand, walk and climb
but limbs could only be used to ‘rake’ small
objects of interest along the floor
• VM group had severe postural abnormalities:
great difficulty walking or sitting. Although
they had some use of the arms they could
not control their shoulders.
Experiments by Lawrence and
Kuypers (1968)
Conclusions:
• the VM tracts are involved in the control of
posture and whole-body movements
• the DL tracts control limb movements (only
the direct tract controls independent
movements of the digits.
The case of H.M.

Intractable epilepsy
one generalized convulsion each week
 Several partial convulsions each day


1953 surgery: Bilateral medial temporal
lobectomy
temporal pole
 amygdala
 entorhinal cortex
 hippocampus

Corkin et al. (1997)
Corkin et al. (1997)
Effects of Bilateral Medial Temporal
Lobectomy
Convulsions were dramatically reduced
 IQ increased from 104 to 118
 Short-term memory (STM) intact
 Temporally-graded retrograde amnesia
 Severe anterograde amnesia

Amnesia
Retrograde (backward-acting) – unable to
remember the past
 Anterograde (forward-acting) – unable to
form new memories
 While H.M. was unable to form most types
of new long-term memories, his STM was
intact

Mirror-drawing task
H.M.’s performance
improved over 3
days (10 trials/day)
despite the fact
that he could not
consciously
remember the task
on days 2 and 3.
Rotary-Pursuit Test
H.M.’s performance
improved over 9
daily practice
sessions; again,
with no recognition
of the experience
Explicit vs Implicit Memories


Explicit memories – conscious memories
Implicit memories – unconscious memories
Repetition priming tests were developed to assess
implicit memory performance;
Incomplete pictures test
Implications of H.M.’s amnesia
Medial temporal lobes are involved in
memory formation.
 STM and LTM are dissociable – H.M. is
unable to consolidate certain kinds of
explicit memory.
 the fact that he could form some memories
suggests that there are multiple memory
systems in the brain.

Medial Temporal Lobe Amnesia

Not all patients with this form of amnesia are
unable form new explicit long-term memories, as
was the case with H.M.
Two kinds of explicit memory:
Semantic memory (general information) may
function normally while episodic memory (events
that one has experienced) does not – they are
able to learn facts, but do not remember doing
so (the episode when it occurred)
Vargha-Khadem et al., (1997)
Studied three children that had bilateral
temporal lobe damage early in life.
 Like H.M., the children could not form
episodic memory, however they did
acquire reasonable levels of factual
knowledge and language ability in
mainstream school.

Effects of Cerebral Ischemia on the
Hippocampus and Memory
R.B. suffered damage to just one part of
the hippocampus (CA1 pyramidal cell
layer) and developed amnesia
 R.B.’s case suggests that hippocampal
damage alone can produce amnesia
 H.M.’s damage and amnesia was more
severe than R.B.’s

Object-Recognition Memory



Early animal models of amnesia involved implicit
memory and assumed the hippocampus was
key
1970’s – monkeys with bilateral medial temporal
lobectomies showed LTM deficits in the delayed
nonmatching-to-sample test
Like H.M., performance was normal when
memory needed to be held for only a few
seconds (within the duration of STM)
Delayed nonmatching-to-sample task
pretend you’re the monkey
Sample stimulus
touch it and get a yummy treat
10 min delay during which other
sample stimuli are presented
Choice phase: pick the image that is new
Darn, no food
Another
yummy treat
Testing object-recognition memory
Medial temporal lobe (MTL)
Delayed non-match to sample results
The Mumby Box
Object recognition in rats
Comparison
of lesions in
monkeys
and rats
Neuroanatomy of object recognition
Bilateral removal of the rhinal cortex
consistently results in object-recognition
deficits.
 Bilateral removal of the hippocampus
produces moderate deficits or none at all.
 Bilateral removal of the amygdala has no
effect on object-recognition.

Is the hippocampus involved in
object recognition memory?
The Case of R.B. suggests that the lesions
of the CA1 region of the hippocampus
(due to ischemia) can produce severe
memory deficits
 Ischemia in animal models also produces
deficits in object recognition
 Yet deficits in object recognition are only
moderate to non-existent in other animal
lesion models
 Why?

Mumby et al. (1996)
Bilateral hippocampectomy actually blocks
the damage produced by ischemia!
Explanation:
 Ischemia causes hippocampal neurons to
release glutamate, which produces
damage outside of the hippocampus
(particularly in rhinal cortex), although
standard histological techniques do not
show the damage follow-up functional
imaging studies have confirmed the
dysfunction.

The Hippocampus
Rhinal cortex plays an important role in
object recognition.
 Hippocampus plays a key role in memory
for spatial location.
 Hippocampectomy produces deficits on
Morris maze and radial arm maze
(Chapter 5)
 Many hippocampal cells are place cells –
responding when a subject is in a
particular place

Theories of Hippocampal Function



O’Keefe & Nadel (1978) Cognitive map theory –
constructs and stores allocentric maps of the
world
Rudy & Sutherland (1992) Configural
association theory – involved in retaining the
behavioral significance of combinations of
stimuli
Brown & Aggleton (1999) is involved in
recognizing the spatial arrangements of objects
Synaptic Mechanisms of Learning
and Memory
What is happening within the brain
structures involved in memory?
 Hebb – changes in synaptic efficiency are
the basis of LTM
 Long-term potentiation (LTP) – synapses
are effectively made stronger by repeated
stimulation

Long Term Potentiation (LTP)
Cross-section of the NMDA receptor complex
Ca2+
NMDA
Glutamate
+
AP-5
Na
D-Cycloserine
Glycine
Polyamine
HA-966
Zn 2+
PCP
Mg
MK-801
2+
Mg 2+
K+