Multiple Choice Flashcards
Downs Syndrome
- Risk increase with mother’s age
- Have 3 copies of chromosome 21
- Characteristic disfigurement, mental retardation, other health problems
- Up to 50% of DS patients die in childhood because of cardiac, kidney, digestive, and immune problems
- 15 x more likely to get leukemia
– Decrease density of axon and dendritic branching, decreased dendritic spines.
- Link to Alzheimer’s Disease.
Epileptic auras
Seizures often preceded by an aura, such as a smell, hallucination, or feeling
suggest the epileptic focus
warns of an impending seizure
Regeneration CNS and PNS
Regeneration is virtually nonexistent in the CNS of adult mammals and unlikely, but possible, in the PNS
Schwann cells promote regeneration
Ogliodendroglia block regeneration
Neurotransplantation
Neurotransplantation = **transferring stem cells to treat neurological damage/disease. **
Fetal Tissue: fetal substantia nigra used to treat MPTP treated monkeys and was successful
Stem Cell:
- adult
- embryonic
- umbilical cord
Experimentally used in Parkinson’s patients, so far so good
Explicit vs. Implicit memory loss
explicit memories – conscious memories
implicit memories – unconscious memories, as when H.M. shows the benefits of prior experience
Korsakoff’s Syndrome
Amnesia, confusion, personality changes, confabulation (making up history/memory), and physical problems
comparable to medial temporal lobe amnesia in early stages
Mostly alcoholics get this.
Medial Temporal Lobe Amnesia
semantic memory may function normally (general info) while episodic memory does not (events experienced)
They can remember facts, but not personal history.
Long Term Potentiation (LTP)
- induction
- maintenence
- expression
only occurs if presynaptic firing is followed by postsynaptic firing
the effects are greatest in areas involved with learning and memory
Chimeric Figures
Chimeric Figures = split pictures
Task for split brain patients, each hemisphere of a split-brain can learn independently and simultaneously
Apraxia
difficulty performing movements when asked to do so out of context, can perform them spontaneously
associated with damage to left hemisphere
Cross Cueing
Non-neural communication between the two hemispheres
How: After incorrect response (LH), shakes head and frowns (RH), changes answer (LH)
Or, after choosing incorrect response with right hand (LH), left hand (RH) grabs the hand away.
Cortical Asymmetries in Language
All of these function primarily in left hemisphere
• Planum temporale (Wernicke’s Area)
– Temporal lobe, posterior lateral fissure
– Language comprehension
• Heschl’s gyrus - primary auditory cortex
• Frontal operculum (Broca’s Area)
– Near face area of primary motor cortex
– Language production
Transcortical Sensory Aphasia
A speech disorder in which a person has difficulty comprehending speech and producing meaningful spontaneous speech
Caused by damage to the region of the brain posterior to Wernicke’s area.
Analytic, motor and linguistic theory (left hemisphere)
Analytic: left is analytic, right is synthetic, vague and untestable
Motory: Left controls fine movement, left damage may produce speech and motor deficits
Linguistic: Primary role of left is language
Genetics and Schizophrenia
Clear genetic basis
– Inherit an increased risk for the disorder
Multiple causes
– Several different chromosomes implicated
– Associated with various early insults
-But not deterministic: identical twin chance is 50%
Appears that interference with the normal development of susceptible individuals may lead to development of the disorder
Positive and Negative Symptoms
POSITIVE SYMPTOMS
thought to be due to overactivity of several types of dopamine receptors
NEGATIVE SYMPTOMS
• thought to be due to brain damage (structural abnormalities)
- degree of brain damage (temporal and frontal lobes) correlated with severity of negative symptoms
- frontal lobes seem particularly affected
Blood flow in mood disorder
Medial Frontal Regions: showed largest difference between control and depressive groups= 12% decrease in blood flow!
Drevets et al.
– Found increase in metabolism in amygdala and medial thalamus (both control emotional behavior) in depressed individuals
– If antidepressant treatment is successful, you see decrease in amygdala neural activity
– However, if antidepressant treatment is unsuccessful • do NOT see decrease in amygdala neural activity
Genetics and depression
Diathesis-Stress Model
• Inherited genetic susceptibility (diathesis) + stress = depression
-Concordance (genetic inheritance) rate is higher for bipolar than unipolar
Diathesis-Stress Model
Inherited genetic susceptibility (diathesis) + stress = depression
• Support is indirect
– Depressed people tend to release more stress hormones
– Fail dexamethasone suppression test
– normal negative feedback on stress hormones not functioning
Types of Anxiety Disorders
- Generalized – stress and anxiety in the absence of a causal stimulus
- Phobic – similar to generalized, but triggered by a stimulus
- Panic disorders – may occur with other disorders, but also alone
- Obsessive-compulsive disorders (OCDs) – obsessive thoughts alleviated by compulsive actions
- Posttraumatic stress disorder
Animal Models of Anxiety
• Assess anxiolytic potential of drugs - assume that defensive behaviors are motivated by fear, and that fear and anxiety are comparable
– Elevated-plus-maze: time in open arms indicates less anxiety
– Defensive-burying: More time burying, more anxiety
– Risk-assessment test: Time freezing and assessing risk indicate anxiety level
Balint’s Syndrome
-Ventral stream “where” damage.
– Bilateral damage to parietal lobes
– Simultanagnosia: Patients have tunnel vision; eyes stay focused on any small object that happens to be in foveal vision & ignores all other objects in vicinity
Simultanagnosia = can’t see simultaneous objects.
Binding Problem
Binding:
- How separately represented pieces of information about one thing are later brought together
- Acheived by synchronized oscillation of neural groups in the brain (basicaly doing the wave)
Attention and Consciousness
Selective Attention (cocktail phenomenon)
Although by no means conclusive, current evidence suggests that…
Top-down attention and perceptual consciousness are two distinct but often allied processes with distinct neurobiological processes.
As a consequence, it will be important to carefully distinguish the neuronal correlates of consciousness from the neuronal correlates of selective attention (Tse et al., 2005).
Organization of sensory system
Sensory areas of the cortex:
- primary = input mainly from thalamic relay nuclei
- secondary = input mainly from primary and secondary cortex within sensory system
- association = input from more than one sensory system, usually from secondary sensory cortex
Somatosensory Agnosias
Produced by large lesions to parietal cortex
- asterognosia = inability to recognize objects by touch
- asomatognosia = inability to recognize parts of one’s own body
Mnemonics: Soma = body
Astero = Astero-glide (touchy touchy :D)
Somatosensory Pathways
The somatosensory system is a diverse sensory system comprising the receptors and processing centres to produce the sensory modalities such as…
touch, temperature, proprioception (body position), and nociception (pain).
The sensory receptors cover the skin and epithelia, skeletal muscles, bones and joints, internal organs, and the cardiovascular system.
Nociception looks like no-ice = pain!
Proprio = body position, such as being propped up.
Types of Brain Tumors
- gliomas = arise form glial cells, half of all brain tumors
- meningiomas = encased or attached to meninges
- infiltrating = grow through surrounding tissue
- metastatic = transfer of cells from one region to another
Meta = bringing tumor to the next level - THE BRAIN!
NMDA Receptors and Glutamate
LTP is mostly commonly studied where NMDA glutamate receptors are prominent
The NMDA receptor (NMDAR), a glutamate receptor, is the predominant molecular device for controlling synaptic plasticity and memory function.
Closed Head Injuries
- Brain injuries due to blows that do not penetrate the skull – the brain collides with the skull
- Concussion – when there is a disturbance of consciousness following a blow to the head and no evidence of structural damage.
- While there is no apparent brain damage with a single concussion, multiple concussions may result in a dementia referred to as “punch- drunk syndrome”
– Contrucoup injuries – contusions are often on the side of the brain opposite to the blow (contra = opposite)
• Contusions – closed-head injuries that involve damage to the cerebral circulatory system. A hematoma forms.
Punch-Drunk Syndrome
While there is no apparent brain damage with a single concussion, multiple concussions may result in a dementia referred to as “punch- drunk syndrome”
Tardive Dyskinesia
Some antipyschotic drugs produce a motor disorder called tardive dyskinesia
It is a disorder resulting in involuntary, repetitive body movements. The involuntary movements are tardive, meaning they have a slow or belated onset.
This neurological disorder frequently appears after long-term or high-dose use of antipsychotic drugs
Apoptosis
Programmed cell death
Biochemical events lead to characteristic cell changes (morphology) and death. These changes include blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, and chromosomal DNA fragmentation.
Neural Degeneration and Regeneration
- Various neurochemicals can block or limit neurodegeneration
- Apoptosis inhibitor protein – introduced in rats via a virus
- Nerve growth factor – blocks degeneration of damaged neurons
- While regeneration does not normally occur in the CNS, experimentally it can be induced
Schwann Cells vs. Oligodendroglia
Schwann cells prmote regeneration
Oligodendroglia actively block regeneration; eliminate inhibition of oligodendroglia and regeneration can occur
Rehabilitative Training
Repairing CNS damage.
Strokes: repetitive training can reduce the spread of neural loss from the core damaged area. Tested via small motor lesions on monkeys, with constant training - limited the damage done.
Spinal injury: patients were supported by a harness while walking on a treadmill. Most people became independent walkers again.
Exercise: reduced age-related decline, and increase neurogenesis in hippocampus (in rats who ran wheels a lot).
Alzheimer’s Disease and Amnesia
Alzheimer’s invoves major anterograde (forward acting) and retrograde (backward acting) amnesia in explicit memory tests; deficits in STM and some types of implicit memory
• Decreased acetylcholine
– Due to basal forebrain degeneration
– Basal forebrain strokes can cause amnesia and attentional deficits which may be mistaken for memory deficits
Memory Reconsolidation
When a memory is retrieved from LTM, it is temporarily held in STM and therefore susceptible to post traumatic amnesia until it is reconsolidated
Z Lens
Advanced study of split-brains with a contact lens to restrict visual input to one hemisphere
Left vs. Right Handers and Brain
92% R.Handers are L.Hemisphere dominant
69% L.Handers are L.Hemisphere dominant
Split Brain Patients
• Corpus callosum
– Largest cerebral commissure
– Transfers learned information from one hemisphere to the other
– When cut, each hemisphere functions independently
• Studying split-brain cats
– transect corpus callosum and optic chiasm so that visual information can’t cross
• Left hemisphere can tell what it has seen, right hemisphere can show it.
Dopamine Theory of Schizophrenia
Side effect of antipsychotic drugs suggested role of dopamine in schizophrenia
In general, the higher affinity a drug has for DA receptors, the more effective it is in treating schizophrenia
MANY problems with this theory
Depression and the Role of Sleep
- More than 50% of depressed patients improve after one night of sleep deprivation.
- Short-lasting: depression returns when normal sleep pattern resumes.
- Not explained by any theory
Brain Areas and NT in OCD
OCD:
- partially genetic
- part of the basal ganglia (caudate nucleus) involved in suppressing impulses appears dysfunctional
- serotonin drugs enhance caudate activity and reduce OCD
Neural Basis for Anxiety
- Drugs suggest a role for serotonin and GABA
- Amygdala, due to its role in fear and defensive behavior, thought to be involved
Blind sight: (What is it)
The ability to respond to visual stimuli even without awareness of that stimuli. E.g., a person will claim to be blind, but they will move out of the way of obstacle (due to scotoma). Can occur via V1 damage.
Kluver Bucy Syndrome
Consumption of almost anything edible (even cigarettes and razorblades) due to lack of temporal lobe. Monkeys who had temporal lobes removed would eat and mount things indiscriminately.
Visual Neglect
People ignore objects in contralateral half of body and left half of space around them ( due to damage to right parietal lobe).
Visual Agnosia
Failure of recognition. Able to see objects, but unable to recognize them. E.g. damage to “what” pathway makes everything look abstract / not recogniable. E.g. John in the train station.
Scotomas
Areas of blindness in visual field – the blind areas are “filled in” by the brain (e.g. clock in blind spot will be ‘replaced’ by a wall). Due to V1 damage, stroke, migraines.
Cutaneous Receptors
Free nerve endings—temperature and pain. Part of somatosensory system.
Somatosensory homunculus:
“Little man.” Map of somatosensory cortex.
Strokes:
Aneurysm , Cerebral hemorrhage, ischemia… and what processes causes most stroke damage?
Aneurysm: weakened point in blood vessel,
Cerebral hemorrhage: bleeding in the brain (no cure).
Ischemia: disruption of blood supply, most common, less severe.
Ischemia causes: Thrombosis (plug forms), Embolism (plug forms elsewhere & moves to brain), Arteriosclerosis (blood vessel thickens due to fat deposits)
Most stroke damage is a consequence of excess neurotransmitter release- especially glutamate (excitatory neurotransmitter), leading to excess sodium and calcium (NA+ CA++)
Drug called t-PA can break up clots - early treatment essential.
Encapsulated verses infiltrating tumor:
_Encapsulated tumor: _Growing within their own membranes= puts pressure on rest of the brain. THey grow outside brain, recovery is usually good. Usually benign, surgically removable.
Most brain tumors are infiltrating. Grow diffusely through surrounding tissue. Malignant, and difficult to remove or destroy
Contusions and hematoma:
Contusion: Closed head injuries that involve damage to the cerebral circulatory system. often on the side of the brain opposite to the blow.
Hematoma: A bruise or collected blood, forms at injury point.
Brain infections: different types
Bacterial Infections:
Syphilis – may produce a syndrome of insanity and dementia known as general paresis. (May be in dormant stage for years)
Viral Infections:
Rabies – high affinity for the nervous system
Mumps and herpes – typically attack tissues other than the brain
Infections can lead to: limiting BLOOD SUPPLY, change oxygen/glucose metabolism.
It can also alter the characteristics of the membrane (electrical properties)
symptoms: lowering blood pressure, severe headaches, nausea, confusion
Neurotoxins : Toxic psychosis:
Chronic insanity produced by a neurotoxin—(Mad Hatter—mercury exposure lead to psychosis
Epilepsy: partial vs. generalized seizures
PARTIAL SEIZURES:
**Simple: **symptoms are primarily sensory or motor or both (Jacksonian seizures). symptoms spread as epileptic discharge spreads
**Complex: **often restricted to temporal lobe (temporal lobe epilepsy) . patient engages in compulsive and repetitive simple behaviors (“automatism”). more complex behaviors seem normal
GENERALIZED SEIZURES:
**Grand mal: **Loss of consciousness and equilibrium. Tonic-clonic convulsions. Rigidity (tonus) and tremors (clonus). Resulting hypoxia may cause brain damage
**Petit mal: **Not associated with convulsions. A disruption of consciousness associated with cessation of ongoing behavior
Neural reorganization and recovery:
Reorganization of primary sensory and motor systems has been observed following damage to peripheral nerves and cortical areas, occurs within minutes. Difficult to distinguish between true recovery and compensatory changes.
Blocking neurodegeneration:
Apoptosis inhibitor protein: Introduced in rats via a virus & blocks loss of hippocampal cells
Nerve growth factor: Blocks degeneration of damaged neurons
Estrogens: Limit or delay neuron death
Neuroprotective molecules tend to promote regeneration
Lashley’s Engram: (Studies on Memory)
Wanted physical representation in the brain of what has been learned, doesn’t matter where cut, but amount cut did matter (learning is everywhere in brain).
Radial arm and Morris Maze:
Radial Arm: Rats put in pool and have to swim to find platform, center location with arms protruding out, some with food—rats learn to only go to food arms._ _hippocampal-damage rats have trouble, often die. :(
- *Morris Maze:** Ability to only visit baited arms of the maze is a measure of reference memory (memory for the general principles and skills required to perform a task.
- *Hippocampus seems to play a role in spatial memory in many species – not just rats.**
Delayed non-matching to sample test (task):
Monkey picks up object to get food underneath, then screen lowers and a new object is added with food under it, normal monkeys pick new object, but medial temporal lobe lesioned monkeys can’t.
Shows importance of medial termporal lobe with learning and memory. Medial temporal lobe damage is related to amnesia as well.
Anterograde verses retrograde amnesia:
Anterograde is forward acting amnesia (can’t from new memories).
Retrograde is backward acting. (can’t remember the past)
Theories of hippocampal function:
- Standard consolidation theory
- Multiple trace theory
- Cognitive map theory
- Configural association theory
- Spatial arrangement theory
1. Standard consolidation theory— Hippocampus temporarily stores memories.
2. Multiple trace theory—Hippocampus stores memories as long as they exist.
3. Cognitive map theory—Collects and stores allocentric maps of the world.
4. Configural association theory—Retains behavioral significance of combinations of stimuli.
5. Spatial arrangement theory—Recognizing spatial arrangements of objects.
What do Cerebral Commissures do?:
Connect two hemispheres of brain (corpus callosum and optic chiasm)
Mnemonic: people meet in a COMMISary
Helping hand phenomenon:
The hand that knows may correct the other in split brain.
In test in which two visual stimuli were presented simultaneously. As right hand reached out to pick up what the left hemisphere saw (orange), the left hand (right hemisphere) dealt with this by grabbing the other hand away from the orange and towards the pencil.
Pure word deafness:
Damage to left temporal lobe
• Produces disorder of auditory recognition
• People are not deaf, but cannot understand speech
• Can recognize non-speech sounds
• Can recognize emotion expressed in speech
• They also have excellent speech
Affective disorders: Causal Factors & Treatment
Depression / bipolar - we know the drill here.
Causes:
Reactive – triggered by negative event
VS.
Endogenous – no apparent cause
Biopsych causes:
- Genetics - Concordance rate higher for bipolar than unipolar. More concordance in identical twins than fraternal twins.
- Stressful experiences - depressives report more stress.
Antidepressant drugs: (MAOI’s, Tricyclic, Monoamine Reuptake Inhibitors, Lithium, SSRI’s)
**• Monoamine oxidase inhibitors (MAOIs): **Prevent breakdown of monoamines (NE and 5HT)… Must avoid foods high in tyramine (e.g., cheese, wine, pickles, etc.) or dangerous drop in blood pressure.
**• Tricyclic antidepressants: **– Block reuptake of serotonin and norepinephrine– Safer than MAOIs, but high dose needed to be therapeutic & can promote weight gain.
- **Selective monoamine reuptake inhibitors: **– E.g., Prozac, Paxil, Zoloft
- Lithium- mood stabilizer
Monamine theory of depression:
Underactivity of serotonin and norapinefrine.
– Consistent with drug effects
– Up-regulation of receptors at autopsy of depressed individuals consistent with this
- Increase in NE and 5HT receptors due to low levels of NT eliciting a compensatory response
- Problem with theory – not all respond to monoamine agonists (only 25% of patients)
Brain damage and unipolar depression:
Damage to amygdale and PFC (involved in perception and experience of emotion.) Consistent with anhedonia.
Treatment of anxiety disorders (medication):
Benzodiazepines ( “Benso’s”, ex: Valium): Also used as hypnotics, anticonvulsants, muscle relaxants. GABAA agonists – bind to receptor and facilitate effects of GABA.
Serotonin agonists (Buspirone, SSRIs): – Reduce anxiety without sedation and other side effects… but Highly addictive
Tourette’s syndrome: Symptoms, Causes, Brain
Symptoms:
1st stage: tics, involuntary movements (face, limbs, or whole body)
2nd stage: inarticulate cries are added to tics
3rd stage: echolalia (repeat what others say) and coprolalia (obscene speech)
Causes: not sure yet. No comparible animals, no identified gene, fMRI scans difficult due to tics.
**Brain: **Abnormality in basal ganglia, thalamus, and cortex feedback circuit.
Treatment: neuroleptics, or deep brain stimulation.
Schizophrenia and brain areas:
(See essay section)
Antipsychotic drugs:
Chlorpromazine/thorazine—calms agitation due to dopamine overactivity.
Haldol—binds to D receptors, neuroleptics like Clozapine
Charles Bonnet syndrome:
• Experience vivid hallucinations in blind spots.
• Damage in visual pathway
• Either completely or partially blind
• Experience vivid, often bizarre visual hallucinations
-replace reality that is missing (e.g. tiny policemen, monkey in lap)
Mnemonic: Charles weirdly hallucinates people wearing BONNETS.
Krick & Koch’s theory of Consciousness:
- Oscillations are neural correlates of experience
- Propose that binding is achieved by synchronized oscillations of neuronal groups in brain
- When 2 pieces of info are bound, then relevant neural groups oscillate with same frequency and phase
- Certain 35-75 hertz oscillations in cortex are the basis of consciousness -Oscillations are correlated with awareness in different modalities
-Suggest mechanism by which binding is achieved.
Mnemonic - Krick the geneticist liked twisty helixes. Krick the psychologist likes twisty oscillations
Capgras-imposter syndrome:
-Intact intelligence / mental processes, but suffer imposter syndrome: Believe that familiar people are imposters (e.g. parents). Also, believe that familiar things such as house, dog, etc. are imposters.
- Occurs in conjunction with traumatic brain injury, Due to a disconnection between the recognition and emotional areas of the brain… e.g. Temporal lobes and the limbic system (amygdale)
- Galvanic Skin Response: no reaction when seeing father’s face.
- Sees familiars as genuine over the phone, due to separate audio pathways.
- Condition tends to heal by itself and goes away
Cotard’s:
All sensory areas are disconnected from amygdala - senses have no emotional connotation—person thinks he or she is dead.
Mnemonic: Dead bodies lie on a COT, tard.
Anosnogia:
Denial of neglect patients—ignore fact that half of body is paralyzed.
Mnemonic: Anosnogia patients do “a -know” that half their body is paralyzed.
Prosopagnosia:
Agnosia for faces and other specifics (cows, chairs).
- Due to damage to ventral “what” pathway.
- Unconsciously recognizes faces at some level, evidenced by increased galvanic skin response.
Somatosensory systems damage: Asterognosia:
Asterognosia—inability to recognize objects by touch.
Mnemonic: Asteroglide is great for touchy touchy :)
Asomatagnosia:
Failure to recognize parts of one’s own body.
Remember, soma = body.
Simultanagnosia:
Difficulty in visually attending to more than one object at a time.A Disorder of attention.
Mnemonic: Simultanagnosia patients canot SIMULTANeously look at two things.
Contrecoup injury:
Injuries (contusions) are often on side of brain opposite the blow.
Neurotoxins (drugz)
Neurotoxic effects of alcohol, some antipsychotic drugs cause tardive dyskinesia.
Some antipsychotic drugs produce motor disorder caused tarditive dyskinesia (involuntary movements)
Recreational drugs, such as alcohol, may cause brain damage
Some neurotoxins are endogenous- produced by the body
