Transcript Chapter 1

CHAPTER 12
Learning
and Memory
Learning deficiencies and Disorders
Learning disabilities
• Much more complex and not really a problem with “learning”
• Learning disabilities categorized either by the type of
information processing that is affected or by specific difficulties
caused by a processing deficit.
• Learning disabilities must include difficulty in
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Input
Integration of information
Storage of information
output
Learning disabilities:
Many forms of LD
• Reading
– 70-80% of learning disabilities
– Dyslexia too broad: just means can’t read or have difficulty reading
– Too many reading specific difficulties
• Writing disabilities or dysgraphia
• Speech/language
– Dysphasias
– Aphasia
– Also include dysgraphia here
• Mathematical or dyscalculia
• Nonverbal learning disorders
• Dyspraxia: difficulty with motor planning/coordination
• Auditory processing disorders
Learning disabilities
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Why? What part of brain involved? Depends on the type of disability
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Frontal lobe disorders:
– Reading, planning, mathematical, reasoning
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Temporal disorders
– Writing, language based
– Nonverbal
– Processing
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Cerebellum and basal ganglia
– Motor control
– Inhibition of competing responses
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Even brain stem
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Processing disorders: disconnect between incoming info and getting to right
part of brain!
Learning disabilities:
How treat
• Must first identify
– Parents often first to identify
– Teachers
– Pediatricians last to notice: not enough interaction
• Assessments
– Variety of standardized tests
– Discrepancy model not really valid anymore
– Examine specific strengths and weaknesses
• Then develop interventions
Learning disabilities:
How treat
• Mastery model:
– Learners work at their own level of mastery.
– Gain fundamental skills before moving onto the next level
– Might include : Direct Instruction
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Highly structured, intensive instruction
Emphasizes carefully planned lessons for small learning increments
Scripted lesson plans
Rapid-paced interaction between teacher and students
Correcting mistakes immediately
Achievement-based grouping
Frequent progress assessments
• Classroom adjustments might include
– Preferential seating assignments
– Alternative or modified assignments
– Modified testing procedures
Learning disabilities:
How treat
• Special equipment:
– Electronic spellers and dictionaries
– Word processors
– Talking calculators
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General use of calculators
– Books on tape
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FM systems
• Classroom assistants:
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Note-takers
Readers
Proofreaders
scribes
• Special Education:
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Prescribed hours in a special class
Placement in a special class
Enrollment in a special school for learning disabled students
individual education plan (IEP)
Dementia
Memory loss and aging
• For many years researchers believed:
– deficits in the elderly caused by a substantial loss of neurons
– Loss was especially from the cortex and the hippocampus.
• More recent investigations
– number of hippocampal neurons not diminished in aged rats
– Even rats with memory deficits show little neuronal loss
– What neuronal loss occurs from cortical areas was relatively minor.
• BUT: certain circuits in the hippocampus do lose synapses
and NMDA receptors as animals age.
– Probably as a result of these changes, LTP is impaired in aged rats.
dementias
• Dementia
– substantial loss of memory and other cognitive abilities
– Typically in elderly
– 50% of those over 80 show some signs of dementia
• Other dementias:
– Frontal-temporal dementia
– Vascular dementias
– Dementias from illness such as stroke/heart attack
dementias
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Alzheimer’s disease
– most common cause of dementia is
– progressive brain deterioration, impaired memory, loss of other mental abilities.
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Earliest and most severe symptom = impaired declarative memory.
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Language, visual-spatial functioning, and reasoning are particularly affected
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Behavioral problems such as aggressiveness and wandering away from home.
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Sundowning:
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increased confusion and restlessness in patients
Behavioral problems begin to occur in the evening or while the sun is setting.
more frequent during the middle stages of Alzheimer's disease and mixed dementia.
subsides with the progression of dementia.
20–45% of Alzheimer's patients will experience some sort of sundowning confusion.
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Alzheimer’s affects nearly 10% of people over 65 years of age, and nearly half of
those over 85.
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http://www.youtube.com/watch?v=MUCO1h48AHM&feature=related
Brain changes in dementia
• There are two notable characteristics of the Alzheimer’s brain,
though they are not unique to the disease.
– Plaques
– Neurofibrillary tangles
• Plaques = clumps of amyloid
– a type of protein
– cluster among axon terminals
– interfere with neural transmission.
• Neurofibrillary tangles
– Abnormal accumulations of the protein tau
– form inside neurons.
– Tangles are associated with the death of brain cells.
Figure 12.14 Neural
abnormalities in the brain of
an Alzheimer’s patient
(a) The round clumps in the
photo are plaques. (b) The
dark twisted features are
neurofibrillary tangles.
Dementia brain changes
• In the Alzheimer’s brain,
– gyri are smaller
– sulci are wider than in the normal brain.
• In the diseased brain, many of the lesions are located in the
temporal lobe.
– Because of their location, they effectively isolate the hippocampus
from its inputs and outputs,
– this partially explains the early memory loss.
• Plaques and tangles in the frontal lobes account for
– additional memory problems
– attention and motor difficulties.
Figure 12.15 Alzheimer’s brain (left)
and a normal brain
The illustrations show the most obvious
differences, the reduced size of gyri and
increased size of sulci produced by cell
loss in the diseased brain.
Ach and memory
• Acetylcholine:
– Neural systems in various parts of the brain that produce
acetylcholine are critical for cognitive functions
– including attention and learning.
• Acetylcholine-releasing neurons are among the
victims of degeneration in Alzheimer’s disease.
• The majority of treatment efforts have focused on
restoring acetylcholine functioning.
– E.g., cognex, aricept, exelon
Drugs for dementia
• Currently five drugs approved by the FDA for
the treatment of Alzheimer’s.
• Four of them improve acetylcholine neurotransmission
by preventing the breakdown of acetylcholine at the
synapses (AchE inhibitors).
• drugs provide only modest relief for both memory and
behavioral symptoms in mild cases of Alzheimer’s
• little or no help when degeneration is advanced.
Drugs for dementia
Generic
Brand
Approve Side Effects
d For
donepezil
Aricept
All stages Nausea, vomiting, loss of appetite and
increased frequency of bowel
movements.
galantamine Razadyne Mild to
Nausea, vomiting, loss of appetite and
moderate increased frequency of bowel
movements.
memantine Namenda Moderate Headache, constipation, confusion
to severe and dizziness.
rivastigmine Exelon
Mild to
Nausea, vomiting, loss of appetite and
moderate increased frequency of bowel
movements.
memantine Namzaric Moderate Headache, diarrhea, dizziness, loss of
to severe appetite, vomiting, nausea, and
+ donepezil
bruising.
Drugs for dementia
• Other drug treatment
– Psychotropic drugs to control behavioral symptoms, reduce
hallucinations
• Haldol, serentil, seroquel, respiridone, mellaril
– Antiseizure medications to control onset of seizures
• Gabapentin (neurotin), dilantin, tegretol
– Tranqulizers and antidepressants
• Ativan, valium, xanax,
• Wellbutrin, lexapro
• Side-effects
– May make lethargic
– May make memory loss greater
– May speed up death
Newer dementia drug
• Memantine: first approved for use in patients with moderate
and severe symptoms.
• Some neuron loss in Alzheimer’s occurs when dying
neurons trigger the release of the excitatory transmitter
glutamate.
– The excess glutamate overstimulates NMDA receptors and kills
neurons, a phenomenon known as excitotoxicity.
– Memantine limits the neuron’s sensitivity to glutamate, reducing
further cell death.
• Studies indicate moderate slowing of deterioration and
improvement in symptoms.
KorsaKoff’s syndrome
• Korsakoff’s syndrome
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Another form of dementia is, brain deterioration
almost always caused by chronic alcoholism.
Typically affects people in 50’s and 60’s
With heavy binge drinking, onset earlier: 20’s and 30’s
• The deterioration results from a deficiency in the
vitamin thiamine (B1), which has two causes:
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The alcoholic consumes large quantities of calories in the
form of alcohol in place of an adequate diet.
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The alcohol reduces absorption of thiamine in the stomach.
KorsaKoff’s syndrome
• The most pronounced symptom : anterograde amnesia
– retrograde amnesia is also severe.
– Impairment is to declarative memory, while nondeclarative memory
remains intact.
• Several brain changes:
– hippocampus and temporal lobes are unaffected.
– mammillary bodies and the medial part of the thalamus are reduced in
size
– structural and functional abnormalities occur in the frontal lobes.
• Thiamine therapy can relieve the symptoms if the disorder is not
too advanced,
• Brain damage itself it irreversible.
KorsaKoff’s symptoms
• Confabulation
– Some Korsakoff’s patients show a particularly interesting characteristic in their
behavior
– Many other dementia patients, particularly frontal-temporal lobe also show this
– They fabricate stories and facts to make up for those missing from their memories.
• Confabulation :
– depends on abnormal activity in the frontal lobes
– confabulating patients usually have lesions there.
• Confabulating amnesic patients
– more trouble than nonconfabulating amnesiacs in suppressing irrelevant information
they have learned earlier.
– Why? confabulation is due to an inability to distinguish between current reality and
earlier memories.
• http://www.youtube.com/watch?v=wDcyBXJAZNM
Eloquent Description of
Dementia
• Dementia is like opening a book of
someone’s life and randomly ripping
individual pages out, one by one, until
there is nothing left but the cover.
– Simon Weisenthal