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Psych370 > Module 2 > Flashcards

Module 2 Flashcards

1
Q

what are the two main purposes of brain damage studies

A
  1. increases our understanding of the healthy brain

2. serves as a basis for the development of new treatments

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2
Q

what were professor P’s main symptoms

A

deafness in his right ear, balance problems, numbers on the right Side of his mouth, trouble swallowing, right tear duct was dry

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3
Q

what did prof P have

A

A tumor sitting on the right 8th cranial nerve (auditory vestibular)

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4
Q

what did prof P’s surgery leave him with

A

permanently deaf and without vestibular function on the right side of his face, hemifacial paralysis, blinking and tearing problems

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5
Q

what are the 5 causes of brain damage in the text

A
  1. tumors
  2. cerebrovascular disorders
  3. closed-head injuries
  4. infections of the brain
  5. genetic factors
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6
Q

what is a tumor, and what is another name for it?

A

Neoplasm, a mass of cells growing independently of the rest of the body

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7
Q

what is an meningioma, how many percent of brain tumours do these make up

A

20%, they grow between the meninges

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8
Q

what type of tumours are meningiomas? what does this mean? (3)

A

Encapsulated tumours - grow in their own membranes

  1. easy to spot in a CT
  2. Can only influence brain function by pressure
  3. almost always benign
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9
Q

what is a benign tumour

A

tumours that are surgically removable with little risk of further growth

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10
Q

what is an infiltrating tumour

A

those that grow diffusely through surrounding tissues

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11
Q

what are most infiltrating tumours, and what is this?

A

Malignant, which is to say they are difficult to remove or destroy, and any remaining cancerous tissue will continue to grow.

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12
Q

what are gliomas? are they mostly benign, malignant? encapsulated, infiltrating?

A

Brain tumours that develop from glial cells, they are infiltrating, malignant, and common

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13
Q

What is a metastatic tumour? what’s the percent of brain tumours they account for?

A

Any tumour that is grown from infiltrating cells and then carried to the brain by the blood stream.

10%

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14
Q

what is the most common origin of metastatic tumours?

A

the lungs

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15
Q

What are the chances of recovering from a cancer that has attacked two or more separate sites?

A

very low.

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16
Q

what are encapsulated tumours that grow on the VIII cranial nerve called?

A

Acoustic neuromas

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17
Q

what is a neuroma?

A

a tumour that grows on nerves or tracts

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18
Q

what is a stroke?

A

Sudden onset cerebrovascular disorders the cause brain damage

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19
Q

what are strokes highly implicated in? (3)

A
  1. 5th leading cause of death
  2. The major cause of neurological dysfunction
  3. leading cause of adult disability
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20
Q

what are the most common consequences of stroke? (4)

A
  1. amnesia
  2. aphasia
  3. paralysis
  4. coma
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21
Q

what is an infarct

A

the dead or dying tissue produced by a stroke

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22
Q

what is the tissue surrounding an infarct called? What will come of this tissue?

A

the penumbra

it may recover, or die, depending on a variety of fctors

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23
Q

what is the primary goal of post-stroke treatment?

A

to preserve the penumbra

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24
Q

what are the two main types of strokes?

A
  1. cerebral hemorrhage

2. cerebral ischemia

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25
Q

what is a cerebral hemorrhage

A

occurs when a cerebral blood vessel ruptures, blood seeps into surrounding neural tissue

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26
Q

what is a common cause of a cerebral hemorrhage?
what are these?
where do they tend to form, and why?

A

Aneurisms, which are pathological balloon like dilations

- form on the wall of can artery at point where its elasticity is defective

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27
Q

What are the two main pathways of aneurisms?

A
  1. congenital (present at birth)

2. result of exposure to vascular poisons / infection

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28
Q

what is cerebral ischemia

A

a disruption of the blood supply to an area of the brain

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29
Q

what are the three main causes of a ischemia?

A
  1. thrombosis
  2. embolism
  3. arteriosclerosis
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30
Q

what is thrombosis

A

a plug called a thrombus forms and blocks blood flow at the site of its formation.
could be formed of blood clots, fats, oils, air bubbles, tumours or any combination of the above

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31
Q

what is an embolism

A

a plug called an embolus is carried by blood from a larger vessel into a smaller one, where it becomes lodged

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32
Q

what is arteriosclerosis

A

walls of blood vessels thicken, narrowing channels, typically due to fat deposits, which eventually leads to the blockage of blood vessels

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33
Q

what is an angiogram?

A

X-ray of blood of lymph vessels, good for viewing strokes (particularly ischemia)

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34
Q

what are the two important properties of ischemia induced brain damage?

A
  1. Takes time to develop - substantial neuron loss begins to be noticeable a day or two later than the blockage first occurs
  2. not equally distributed throughout the brain, certain areas in the hippocampus are most susceptible
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35
Q

which neurotransmitter plays a role in ischemia? how?

A

glutamate (very excitatory).

  • after bv becomes blocked, the blood deprived neurons become over-excited and release allot of glu.
  • this in turn over activates glutamate receptor in post-synaptic neurons (these receptors are the NMDA receptors)
  • lots of Na+ and Ca2+ ions enter post synaptic neurons, the excessive concentration of which affects the post synaptic neurons in two ways (later card)
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36
Q

what are the 2 ways excessive Ca2+ and Na+ ions in post synaptic neurons follow ischemia harm them?

A
  1. trigger further release of excessive glutamate, which furthers the toxic cascade
  2. trigger a series of internal reactions that ultimately kill these neurons
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37
Q

what is an implication of the discovery of the role of glutamate in strokes?

A

possibility of preventing stroke related brain damage by blocking the glutaminergic cascade, for example by using NMDA receptor antagonists is clinically effective, but need to be administered right after stroke, which makes them impractical

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38
Q

what are the 2 treatments that have been found to be effective in treating stroke?

A
  1. NMDA receptor antagonists (impractical, need to be administered right after the stroke.
  2. tissue plasminogen activator - breaks down blood clots
    - if administered within 3-4 hours, leads to better recovery
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39
Q

what are the three symptoms that indicate that a blow to the head should be taken seriously/

A
  1. confusion
  2. sensorimotor disturbances
  3. loss of consciousness
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40
Q

what is a contusion

A

a closed head injury that involve damage to the cerebral circulatory system, which produces internal hemorrhagic

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41
Q

what does internal haemorrhaging lead to?

A

a hematoma, which is a localized collection of cloned blood in can organ or tissue (a bruise)

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42
Q

what do closed head injuries result from? where does the blood from such injuries usually accumulate

A

the brain coming into contact with the skull.
Typically in the subdural space, the space between the dura matter and arachnoid membrane, which can severely distort the surrounding neural tissue

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43
Q

what is a countercoup injury? are they common?

A

a contusion that occurs on the opposite side of the blow, and yes

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44
Q

what is a concussion

A

disturbance in consciousness following he’d trauma where there is no evidence of a contusion or other structural damage

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45
Q

what does the recent evidence surrounding concussions suggest?

A

their effects may last many years and the effects of repeated concussions can accumulate

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46
Q

what is CTE (give its full name, and symptoms)

A

Chronic traumatic encephalopathy.
the dementia and cerebral scarring observed in athletes and other people who have experienced repeated concussive or subconcussyve blows to the head

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47
Q

whaat did the Riley et all article conclude about the number of retired American football players with CTE

A

out of 35 studied, 34 had it

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48
Q

what are some common behavioural symptoms associated with CTE?

A

recklessness, gambling, addiction, violent outbursts

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49
Q

how do we diagnose CTE?

what is present in these cases?

A

autopsy, usually by finding aa proliferation of neurofibrillary tangles

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50
Q

what is a brain infection

A

invasion of the brain by micro organisms

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51
Q

what its he inflammation that results from a brain infection called

A

encephalitis

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52
Q

what are the two common types of brain infections

A
  1. bacterial

2. viral

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53
Q

what do bacterial infections typically cause (2)

A
  1. cerebral abscesses - pockets of puss in the brain

2. Meningitis - inflammation of the meninges

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54
Q

what is the percentage of adults that meningitis is fatal in?

A

30%

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55
Q

what treatments can be effective against bacterial infections>

A

penicillin and other antibiotics, can eliminate the infection but CANt reverse damage

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56
Q

what is syphilis?

  1. bacterial or viral?
  2. name of the associated psychotic illness
A

aa bacterial brain infection, passed to new hosts through contact with genital sores. tends to go dormant before becoming virulent and attacked many parts of the body, resulting in the brain in general paresis, a syndrome of mental illness and dementia

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57
Q

what are the two types of viral infections in the brain

A
  1. those with a particular affinity for neural tissue

2. those that attack neural tissue with no special affinity for it

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58
Q

What is rabies

A

a viral infection with a particular affinity for neural tissue, causing increased aggression to lead to biting which transmits it, it takes about aa month before it attacks the brain so we can vaccinate

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59
Q

what is the mumps / herpes examples of?

A

viruses that can attack the nervous system but have no affinity for it

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60
Q

what are we now beginning to suspect in regards to the role of viral infections in the ethology of disorders?

A

probably more than thought, hard to recognize because of the fact that they can lie dormant for so long.

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61
Q

what are the ways neurotoxic chemicals can enter general circulation? (3)

A

From the GI tract, the lungs, or the skin

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62
Q

which types of metals can be harmful to the nervous system?

A

heavy ones, like mercury

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63
Q

what is toxic psychosis

A

the permanent brain damage and associated psychological impairment caused by the accumulation of toxic chemicals in the brain

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64
Q

which types of psychotropic medications are neurotoxic?

A

Some older (and newer lol) antipsychotics which can cause tar dive dyskinesisa

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65
Q

what is tar dive dyskinesiaa

A

primary symptoms - involuntary smacking, sucking movement of the lips, thrusting and rolling of the tongue, lateral jaw movements, puffing of the cheeks

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66
Q

what are endogenous neurotoxins

A

those produced by the patients own body, typically antibodies that attack particular components of the NS, but also some excessive neurotransmitters (like in the case of ischemic stroke and glutamate)

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67
Q

are most genetic factors resulting in brain damage due to recessive or dominant genes?

A

recessive, easier to get passed along

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68
Q

what are the two reasons we haven’t been able to identify and discover effective treatments for the offending genes in all neuropsychological disorders? (2)

A
  1. numerous loci on human chromosomes have been assoc. with each disorder
  2. 90% of chromosomal loci involved in neuropsych disorders are not conventional protein coding genes, they were on poorly understood sections of genes
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69
Q

How does Apoptosis play a role in brain damage?

A

all of the other six causes of brain damage discussed in the text produce damage in part by activating apotpotic mechanisms

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70
Q

what was the early assumption about how cells died following brain damage? what is it now believed to be?

A
  • thought to be purely necrotic
  • now we know that if the damage isn’t incredibly severe, the cells will attempt to activate apoptosis
  • not an either or situation, can show signs of both
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71
Q

explain the necrotic mechanism. how long does this take? what does it cause?

A
  1. damaged neurons swell and bark apart, beginning in the axons and dendrites, ending in the cell body
    - few hours (fast)
    - inflammation
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72
Q

explain the apoptotic mechanism. how long does this take? what does it cause?

A
  1. shrinkage of cell body, packaged into vesicles,
    - slow (day or two)
    - no inflammation, reduced damage to nearby tissues.
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73
Q

what its he primary symtopom of epilepsy? do all people who have these have epilepsy?

A

seizures, no, some one time seizures cn be triggered by exposure to convulsive toxins or high fevers

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74
Q

what is the diagnosis of epilepsy restricted to?

A

those who have seizures that are repeatedly generated by their own chronic brain dysfcuntion

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75
Q

what is the prevelance of epilepsy?

A

3.8% lifetime

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76
Q

are all seizures motor? what do we call motor seizures?

A

no, most are behavioural, cognitive, or emotional that are difficult to isolate from normal activity.
motor seizures are colvulsions

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77
Q

what are the 4 main etiological pathways of epilepsy?

A
  1. there are over 100 faulty genes,
  2. any of the causes of brain damage
  3. faults in inhibitory synaptses (GABAnergic), causing many neurons in a given area to fire in synchronous bursts
  4. inflammation
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78
Q

how do we diagnose epilepsy?

A

EEG, as epilepsy is associated with bursts of high amplitutde EEG spikes, often punctuating the scalp EEG of epileptics between seizures

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79
Q

what is an epileptic aura

A

peculiar psychological changes that occur just before a seizure

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80
Q

why are epileptic auras important? (2)

A
  1. provide clues about the location of the epileptic focus

2. warn patients of impending seizures

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81
Q

what are the two general categories of seizures?

A
  1. Focal

2. generalized

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82
Q

what is a focal seizure? Describe the pattern of neuronal firing.

A

a seizure that does not involve the entire brain.
focal epileptic neurons being to discharge together (synchronous, thus the EEG) in bursts, which tends to spread to other areas in the brain, but not to all areas of the brain in focal seizures.

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83
Q

what are the typical symptoms of focal seizures?

A

depend on the area they begin in, and where they spread, but they tend not to be accompanied by a total loss of consciousness or equilibrium, because they dont spread into the entire brain

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84
Q

what are the two major categories of focal seizures?

A
  1. simple partial

2. complex partial

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85
Q

what is aa simple partial seizure?

A

a focal seizure who’s symptoms are primarily (sensory v motor), often called Jacksonian seizures.
as the epileptic discharges spread throughout the sensory / motor brain areas, the symptoms spread systematically throughout the body

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86
Q

what is a complex partial seizure?

A

Often restricted to temporal lobes (thus called temporal lobe epilepsy), in which the patient engages in compulsive, repetitive and simple behaviours called automatisms, or more complex behaviours that seem normal

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87
Q

do patients tend to remember their complex partial seizures?

A

no, even though they are conscious during them

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88
Q

what is the percentage of cases of epilepsy that are complex-partial in nature?

A

bout half, the temporal lobes are particularly susceptible to epileptic discharge

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89
Q

what are generalized seizures?

A

those that involve the entire brain.

90
Q

where do generalized seizures originate?

A

some begin as focal discharges that spread to the entire brain, others begin simultaneously throughout.

91
Q

what are the two possible causes of generalized seizures that commence in the entire brain simultaneously?

A
  1. diffuse pathology

2. begin focally in a structure that projects to many parts of the brain (such as the thalamus)

92
Q

whaat is the tonic-clonic seizure? (7)

A

primary symptoms - loss of consciousness, equilibrium, violent tonic-clonic convulsions (contracting-stretching convulsions), tongue biting, urinary incontinence and cyanosis (turning blue due to excessive extraction of blood during the seizure) and hypoxia

93
Q

what does the hypoxia in tonic-clonic seizures result in? what is it?

A
  • shortage of oxygen supply to a tissue (in this case, the brain), and can result in brain damage
94
Q

what is the absence seizure?

A 
- not associated with convulsions
primary Behavioural symptoms 
- disrupting of consciousness (cessation of ongoing behaviour)
- vacant look
- fluttering eyelids
95
Q

How is the EEG of the absence seizure different than the other forms?

A

it is bilaterally symmetrical, and a 3 per second spike and wave discharge

96
Q

when are absence seizures most common?

A

in childhood, they tend to cease at puberty.`

97
Q

is there aa cure for epilepsy?

A

no, but we can treat the severity and frequency with anti-epileptics, although these can have negative side effects and dont work for everyone

98
Q

what are some non anti-convulsive treatments for epilepsy? (4)

A
  1. Stimulation of the vagus nerve
  2. transcranial mag stim
  3. ketogenic diet
  4. brain surgery, if all other options have been exhausted
99
Q

what is the prevalence of Parkinson’s over 55, and is it more male or female?

A

movement disorder of middle and old age affecting 1% of those older than 55, with slightly higher prevalence in males than females

100
Q

what are the most common symptoms of full blown Parkinson’s (6)

A
  1. pronounced tremor during inactivity but not during voluntary movement and sleep
  2. muscular rigidity
  3. difficulty initiating movement
  4. slowness of movmeent
  5. masklike face
  6. pain and depression, often before motor symptoms reach full severity.
101
Q

is Parkinsons always associated with dementia?

A

no, it is sometimes but many times their cognitive functions do not impair while they lose control over their bodies

102
Q

what are the causes of Parkinsons? (6)

is there a family history in this disorder?

A
  1. faulty Dnaa
  2. Brain infections
  3. stroke
  4. tumours
  5. traumatic brain injury
  6. neurotoxins
    all implicated in cases, but no cause is obvious. there is no family history of the disorder, although numerous genes have been implicated
103
Q

where is degeneration in Parkinsonism most severe?

A

Substantia nigra (midbrain nucleus) whose neurons project via the nigrostriatal pathway to the striatum of the basal ganglia.

104
Q

what is the neurotransmitter normally emitted from the substantial nigra that is greatly decreased in Parkonsonism

A

dopamin, there is very little in the sub. nigra and striatum

105
Q

what do autopsys of parkinsons patients tend to reveal?

A

Lewy bodies - clumps of protein in the surviving dopaminergic neurons of the sub nigraa

106
Q

what is a medication that haas been known to alleviate Parkinsonism? is it a permanent solution? why or why not?

A

L-Dopa, no.

- becomes less and less effective over time until its side effects (like involuntary movement) outweigh its benefits

107
Q

What are other drugs that help in parkinsons? are they permanent solutions?

A

Dopamine agonists, no, just like L-Dopa they stop working after awhile

108
Q

what does the evidence suggest about the degree of brain damage that has occurred in a parkinsons patient once symptoms present?

A

irreparable brain damage has already occurred, which may be why nothing can fully stop it

109
Q

what is aa controversial treatment of parkinsons?

A

Deep brain stimulation, low intensity electrical current is applied to an area of he brain through a stereotypically implanted electrode

110
Q

what does deep brain stimulation in parkinsons target?

A

Typically, through chronic bilateral electrical stimulation, it targets the nucleus that lies beneath the thalamus that is connected to the basal ganglia (subthalamic nucleus)

111
Q

how does deep brain stimulation work in parkinsons?

A

by blocking the function of the target structure as a lesion would. symptoms tend to be alleviated within seconds of the device being activated, although its effectiveness slowly declines in the following months, and if stimulation is turned off, the improvements dissipate fast

112
Q

are there side effects to deep brain stimulation in parkinsons?

A

yes, such as cognitive, speech and gait problems

113
Q

what is huntingtons

A

a progressive motor disorder with a dimple genetic basis that is always associated with dementia

114
Q

what is the first clinical sign of Huntington’s?

A

increased fidgetiness

115
Q

what are the symptoms that arise as Huntington’s develops?

A
  1. rapid, complex jerky movements of entire limbs rather than specific muscles
116
Q

what are the inevitable consequences of Huntington’s?

3

A

severe motor and intellectual decline (incapable of feeding themselves, controlling bowels, recognizing their kids)
no cure
death within 15 years of appearance of the first symptoms

117
Q

what is the causes of Huntington’s?

A

a single mutated dominant allele called a Huntington, coding for a Huntington protein

118
Q

why can huxngtingtons be passed along despite being dominant?

A

because its symptoms tend to arise after the age of 40, so many people dont know they have it until after they’ve had kids

119
Q

do we have method of testing to see if the offspring of a person with Huntington’s will develop the disorder? what is their likelihood of doing so?

A

yes, 50/50

120
Q

what is Multiple sclerosis

A

progressive disease that attacks the myelin of axons in the CNS, commonly attacking people in their early adulthood

121
Q

what are the neural stages of MS progression? (3)

A
  1. microscopic areas of degeneration on myelin sheaths
  2. damage to myelin so severe that associated axons become dysfunctional, degenerate
  3. areas of hard scar tissue develop in the CNS
122
Q

What is MS considered to be?

which animal model did we discover this in?

A

an autoimmune disorder, as the myelin is attacked by a faulty immune response, was discovered in the animal model of MS called experimental autoimmune encephalomyelitis

123
Q

what is the animal model of MS called?

how do we cause it?

A

experimental autoimmune encephalomyelitis

- by injecting lab animals with myelin and a preparation that stimulates their immune systems.

124
Q

does all damage to axons and neurons in MS occur as a function of demyelination?

A

nope, some occurs without it

125
Q

why is diagnosing MS difficult?

A
  1. nature and severity depend on a variety of factors like…
    - number
    - size
    - location
    of sclerotic lesions
  2. some cases have long periods of remission during which patients seem normal ,although these abet
126
Q

what are the common symptoms of advanced MS? (5)

A
  1. visual disturbances
  2. muscular weakness
  3. numbess
  4. ataxia (loss of motor coordination)
  5. cognitive deficits and emotional changes (in some patients)
127
Q

what are the puzzling features of the epidemiology of MS? (4)

A
  1. genetic factors play less of a role than in other disorders (only 25% concord btwn monozygotic, 5% in dizygootics)
  2. incidence of MS is higher in females than males
  3. incidence is higher in whites than other ethnic groups
  4. incidence is higher in those who live in colder climates, especially during childhood.
128
Q

what are the risk factors for MS? (3)

A
  1. vitamin D deficiency
  2. exposure to the Epstein Barr virus Most common cause of mono)
  3. smoking darts
129
Q

what drugs were introduced to help with MS? how effective are they?

A

Immunomodulatory drugs, their benefits are marginal and only work with some patients

130
Q

what is the most common cause of dementia in the elderly?

A

Alzheimers

131
Q

when does Alzheimers present at its earliest? how is it associated with aging

A

sometimes as young as 40, but likely hood grows with age, about 10% of people over 65 suffer

132
Q

Describe the progression of Alzheimers
early (3)
intermediate (4(
Advanced (1)

A
  1. early - selective decline in memory, deficits in attention, personality changes
  2. intermediate - confusion, irritability, anxiety, deterioration of speech
  3. advanced - deterioration to the point that the most simple of responses are difficult
  4. terminal
133
Q

how do we diagnose alzheimers?

whaat are the new methods that improve early diagnosis? (2)

A

autopsy, since it isn’t the only cause of dementia we can never know until death.

  1. cerebrospinal fluid tests
  2. brain imaging tests
134
Q

what are the three primary physiological indications of Alzheimers disorder?

A
  1. neurofibrillary tangles
  2. amyloid plaques
  3. neuron loss
135
Q

what are neurofibrillary tangles

what part of the cell do we find them in?

A

threadlike protein tangles in the neural cytoplasm

136
Q

what are amyloid plaques

A

clumps of scar tissue composed of degenerating neurons and aggregates of the beta-amyloid protein

137
Q

why are researchers investigating the role fo neurovascular factors in alzheimers

A

because of the presence of small lesions that seem to be due to microhemorrhages called microbleeds

138
Q

are the three physiological markers of alzheimers found throughout the brain?

A

yes, but they tend to distribute mostly in the medial temporal lobe structures

139
Q

which medial temporal lobe structures are the three physiological markers of alzheimers found most specifically in? (3)
what is their dominant overlapping cognitive role?

A
  1. entorhinal cortex
  2. amygdaala
  3. hippocampus
    all involved in memory
140
Q

what three cortical structures are the three physiological markers of alzheimers found most specifically in?

A
  1. inferior temporal cortex
  2. posterior parietal cortex
  3. prefrontal cortex
    all mediate complex cognitive functions
141
Q

what is the genetic component of Alzheimers

A

people with someone who suffers in their immediate family are 2x more likely to get it

142
Q

have there been any genetic mutations found in Alzheimers?

A

yes, but only three, which are implicated in only 1% of the late onset version

143
Q

are there genes implicated in late onset Alzheimers? how many? which is the most notable?

A

yes, about 15

- gene on chrom 19 that codes for the protein APOE

144
Q

why is APOE notable in Alzheimer’s?

what are the assumed mechanisms?

A

An allele of Apoe (apoe4) has been shown to increase susceptibility of late onset form of Alzheimers by 50%
thought to be due to the fact that APOE binds to beta-amyloid, which reduced beta amyloid clearance and could cause its intense aggregation

145
Q

what is a factor complicating the search for aa cure for Alzheimer’s

A

the fact that we dont know what its primary symptom is and a good treatment is dependent on our ability to focus on the primary symptom

146
Q

what is the amyloid hypothesis

A

the dominant view of the primary Alzheimers symptom.

- argues that amyloid plaques are the primary symptom and cause the others

147
Q

what is the main support of the amyloid hypothesis

A

genetic analysis of families with early onset Alzheimers

- all three gene mutations ins the early onset form influence the synthesis of beta amyloid

148
Q

what is the main argument against the amyloid hypothesis

A

many folks without notable dementia have significant amount of amyloid plaques (high plaque normals)

149
Q

what does recent evidence about high plaque normals suggest

A

that they are at an increased risk for cognitive decline and Alzheimer’s

150
Q

what were the first treatment attempts for Alzheimer’s

A

focussed the declining acetylcholine levels as an early indicator of the disorder. cholinergic agonists are still prescribed sometimes, but have proven ineffective except for some mild imrpoivemnts in the early disorder

151
Q

what has been the issue with animal models in Alzheimer’s treatments

A

many treatments found to be effective in animals have not worked on humans

152
Q

what are the tw points of view surrounding the failure of animal models to provide a treatment for Alzheimer’s

A
  1. challenge the amyloid hypoehtis

2. belief that treatments need to be commenced before disease onset or at least in its earliest stages

153
Q

why is the belief that treatments need to be prescribed early on in Alzheimer’s problematic

A

bc most people the seek treatment come in wh en there is already severe brain pathology, which is why early diagnosis is so crucial

154
Q

what have recent clinical trials shown about Alzheimers treatment?

A

that administration of antibodies for beta-amyloid can slow progression

155
Q

which syndrome have we recently focussed on in terms of Alzheimer’s neural mechanisms?
why?

A

Down syndrome,

  1. by 40 almost all people with Down syndrome have developed amyloid plaques and neurofibrillary tangles,
  2. by 60, 2/3 of those with Down syndrome will have dementia.
  3. the gene that codes for beta amyloid resides on chromosome 21, so the hypothesis is that the extra chromosome 21 leads to greater prod of beta-amyloid
156
Q

what has new research demonstrated about the 21 chromosome in those with Alzheimer’s

A

almost 15% of neurons in the brain have 3 copies of 21

157
Q

what is the new hypothesis of Alzheimer’s

A

pathogenic spread,m which proposes that many common neurodegenerative diseases such as Alzheimer’s and Parkinson’s result from the presence of misfiled proteins that initiate aa chain reaction that causes other proteins to misfold, which can cause plaques to form.

158
Q

what are the ways we dont want to think of animal models of disease

A

as though they perfectly replicate human illnesses

159
Q

what is the kindling phenomenon,
where do we usually target?
what does it mirror

A

progressive development and intensification of convulsions elicited by a series of periodic low-intensity brain stimulations, typically daily and in the amygdala
- epilepsy

160
Q

is kindling specific to mice?

A

no, it has been found in rabbits, cats and dogs as well as primates

161
Q

does kindling only occur in the amygdala? must it be caused by electric shocks?

A

no, it can be created in many brain regions, and can also be caused by repeated doses of sub convulsive doses of convulsive chemicals

162
Q

what are the two important features of kindling

A
  1. neurplaastic changes underlying kindling are permanent
  2. kindling is produced by distributed as opposed to massed stimulations (can’t yield it as efficiently if they are reaadministered fast)
    - shorter than a few hours - need more reps
    - less than 20 mins - won’t happen at all
163
Q

what are the two ways kindling models epilepsy

A
  1. convulsions elicited are similar to those in humans with epilepsy in many ways
  2. comparable to epileptogenesis (the genesis of epilepsy) that can follow head injury
164
Q

explain epileptogenesis

- why does it occur?

A

some people who seem to have escaped a nasty head injury may benign to experience convulsions a few weeks later, and they can begin to recur more and more frequently and with more and more intensity

165
Q

what is the important aspect that kindling does not model epilepsy?
is this always the case, even once it begins?

A
  • kindling convulsions are elicited, not spontaneous like epilepsy
  • however, if subjects are kindled a lot (300 times in rats) then they begin to display spontaneous seizures and will continue to do so after they are no longer been g kindled
166
Q

what does transgenic mean?

A

animals into which genes of another species have been introduced

167
Q

what are our most common models for Alzheimer’s

how do we induce this

A

transgenic models, where we insert gene mutations that promote the build up of human beta-amyloid into newly fertilized mouse eggs

168
Q

what happens to mice that are used as transgenic models for alzhiemers when they mature (3)

A
  1. they tend to contain many amyloid plaques like those in human patients with the illness,
  2. the distribution of these plaques is comparable to that observed in human patients (most in medial temporal lobes).
  3. they display neural loss and memory disturbances
169
Q

what is an issue with transgenic models of Alzheimers.

have we figured this out?

A

do not display neurofibrillary tangles (very bad if this is the primary symptom)
yes, by injecting another gene mutation that promotes the accumulation of the Tau protein

170
Q

describe the case of the frozen addicts

A

buncha junkies came in with parkonsonism after doing a bunch of synthetic heroin as a result of MPTP

171
Q

what were the specific symptoms presented by the frozen addicts (5)
(2 are very specific to Parkinsonism)

A
  1. bradykinesia (slow movement)
  2. tremor
  3. muscle rigidity
  4. seborrhoea (oily skin)
  5. Micrographia (small handwriting)
172
Q

do primates exhibit the same effects of MPTP (3)

A

yep, they display parkinsonian symptoms, cell loss in the substantial nigra, major reduction in brain dopatmine

173
Q

do rats exhibit the same effects of MPTP? Mice?

A

No, they are resistance, while mice vary from strain to strain

174
Q

How haas the MPTP model proven useful?

A

Instrumental in the development of many treatments, mainly dopaminergic drugs

175
Q

what is neural degeneration, what is it a component of?

A

neural deterioration and death

component of dev. and disease

176
Q

what is neural degeneration influenced by (3)

A

nearby glial cells, activity of degenerating neurons, particular cause of degeneration

177
Q

how do we induce neural degeneration in the lab?

A

by cutting axons (axotomy)

178
Q

what are the two results of axotomy?

A
  1. anterograde degeneration

2. retrograde degeneration

179
Q

what is anterograde degeneration

A

degeneration of the distal segment (segment of aa cut axon from the cut to the synaptic terminal)

180
Q

what is retrograde degeneration

A

degredation of the proximal segment - segment of a cut axon from the cut to the cell body

181
Q

how does anterograde degeneration occur?
fast or slow? How long?
why?

A

quickly, since the cut separates it from the cell body which is the metabolic centre of the neuron, with the entire distal section becoming stolen in a few hours, breaking into fragments in a few days

182
Q

what is the course of retrograde degeneration?

does it always lead to neuron death?

A

progresses gradually back from the cut too the cell body
takes about 2-3 days b4 major changes are noticeable
these changes are either regenerative or degenerative,

183
Q

what do regenerative early changes in retrograde degeneration look like?
what does this indicate?
do these guarantee its survival?

A

can be an increase in size, etc.
indicates
the cell body is involved in a synthesis of proteins that will be used to replace the damaged axon
doesn’t always guarantee long term survival, as it still needs to make appropriate contact with a post synaptic neuron

184
Q

what do early degenerative changes in retrograde degeneration look like? (1)
what does this indicate? (1)

A

typically a decrease in size or otherwise, and they indicate that its gonna fuckin die

185
Q

can degeneration spread from one neuron to neighbouring ones? what is this possible process called?

A

yes, to those linked by synapses, called transneuronal degeneration.

186
Q

what is anterograde transneuronal degeneration?

A

when degradation spreads from damaged neurons to those on which they synapse

187
Q

what is retrograde transneuronal degeneration.

A

when it spreads from damaged neurons to those that synapse onto them

188
Q

what is neuraal regeneration, and is it good in mammals?

A

the regrowth of damaged neurons, and no it sucks, better in lower vertebrates and invertebrates

189
Q

which sections of the NS allow for regeneration?

A

Only the PNS, but its hit or miss

190
Q

when does regeneration in mamalian PNS begin to occur? what needs to occur before this can happen

A

2 too 3 days after dmg, usually once new growth cones have formed

191
Q

what are the three possible outcomes of the commencement of neural regeneration
1

A
  1. if the og Schwann cell myelin sheath remain intact, the regenerating axons grow through them to their og target at a few mm a day
  2. if its severed and separated by a few mm, then the axon tips often grow into incorrect sheaths and are then guided to incorrect destinations, which is why its hard to regain coordination of limbs after nerve daamage
  3. if the cut ends of the axon become widely separated or if a large section is damaged, there is often no regeneration, and the axon tips develop into a tangled mass around the proximal stump, neurons die
192
Q

is there something inherent about the PNS neurons that allow them to regen?

A

no, if PNS nerves are implanted into the CNS they dont regeneration and vice versa, which indicates that its something about the environment

193
Q

what difference in environment between the PNS and CNS allows for regeneration in the former but not the latter
make new cards for this shit bitch - too much!!

A

Schwaann cells vs oloigodendrogliaa

  • Schwann in PNS clear debris and scar tissue after dmg and promote regeneration by producing neurotrophic factors and CAMS, which stimulate the growth cones of new axis and mark paths along which regeneration axons grow, respectively
  • Oligodendroglia in the CNS do not clear debris or stimulate or guide regeneration, they seem to release facrtorst hat actively block regeneration
194
Q

what is a secondary factor that prevents CNS Regen

what are the two ways they do so?

A

astrocytes form Glial scars, which presents a physical barrier to axonal regrowth, and release regrowth inhibitors

195
Q

what is collateral sprouting

A

the phenomenon that occurs when axon beaches from healthy neurons synapse at the sites that dying neurons leave open.

196
Q

where can the axons in collateral sprouting sprout form?

A

axon terminal branches or nodes of randivier

197
Q

why do most studies on neural reorganization focus n the sensory and motor cortex?

A

bc they are topographically oriented

198
Q

what are the 2 conditions under which we study cortical reorganization?

A
  1. damage to peripheral nerves

2. damage to cortical areas themselves

199
Q

What did the Kaas and colleagues study on neural reorganization show?

A

assessed the effect of making aa small lesion in one retina and removing the other.
months later, the primary visual cortex neurons that had receptive fields in the damaged area of the retinal were found t have receptive fields in the area of the retina next to the lesion, a process which began within minutes of the lesion

200
Q

What did the Pons and colleagues study on neural reorganization show?

A

mapped the primary somatosensory cortex of monkeys who’s arm sensory neurons had been cut 10 years earlier/
cortical face representation had expanded into the original arm area
scale was a massive, had expanded by over a cm

201
Q

what did the saunas super and denghue study on neural reorganization show?
this is clearly the wrong name for these people

A

transcected motor neurons that controlled rat whiskers, then stimulated the area of the motor cortex that had previously been for those a few weeks earlier, which now activated other areas of the face

202
Q

what happens in the sensory maps of blind people?

A

their other senses take over the structures, which results in greater ability in those modalities

203
Q

what are the two mechanisms of neural reorganization?

A
  1. strengthening of existing connections, maybe through release form inhibition
  2. establishment of new connections by collateral sprouting
204
Q

what is the evidence that neural reorganization is accomplished through the strengthening of existing connections, maybe through release form inhibition? (2)

A
  1. reorg often too fast to be explained by growth

2. rapid reorg never involves changes of more than 2 mm of cortical surface

205
Q

what is the evidence that neural reorganization is accomplished through the establishment of new connections by collateral sprouting?

A

the magnitude of long term reorganization can be too great to be explained by changes in existing connections

206
Q

are there other possible mechanisms for neural reorganization? (4)

A

yes, neural degradation, adjustment of dendritic trees, adult neurogenesis, and may not be mediated by the damaged area itself

207
Q

why is studying CNS functional recovery difficult?

A
  1. improvements re modest at best
  2. compensatory changes can be confused with it, ex after cerebral edema, any changes in the following few weeks re due to a decline of swelling and any changes there after could be due to cognitive nd behavioural strategies (Subing functions)
208
Q

when is recovery most likely?

A

when patients are young and lesions are small

209
Q

what is cognitive reserve?

A

education and intelligence, thought to play a role in improvements after brain damage that do not result from actual recovery of function
- allowed for them to find alternative ways of doing things
explains why highly educated people are less susceptible to the effects of brain deterioration in aging

210
Q

does adult neurogenesis contribute nat all?

A

yes, migration of stem cells to damaged areas has been shown in some studies. but there is not evidence that they can migrate all the way from the hippocampus and subventricular zone to distance areas, and no direct evidence they contribute in humans

211
Q

what were the positive early signs of neurotransplantation in Parkinson models (MPTP monkeys?) (4)

A
  1. fetal subnstantia nigra transplants survived,
  2. innverated adjacent stratal tissue,
  3. released dopamine
  4. alleviated the severe poverty of movement, tremor and rigidity
212
Q

what did the neurostransplantation procedure do to humans

A

seemed okay at first, but then they started to display a variety of writhing and chewing movements about a year after surgery

213
Q

what were the two positive results of the failed neurotransplantation study in Parkinson patients

A
  1. curtailed premature clinical use of neurotransplantation in human patients
  2. stimulated reserharcers to look at the effects of various kinds of neurotransplantations in animal models to answer fundamental questions
214
Q

what is the second approach to neurotransplantation research

explain the Xu and colleagues study that demonstrated this effect

A

implanted nonneural cells to block degeneration or to stimulate and guide regen.
- prod cerbral ischemia in rats, produced deficits in the Morris water maze and have dmg to the hippo
teated with viruses genetically engineered to release apoptosis inhibitor protein, which reduced loss of hippo neurons and. deficits in performance

215
Q

what are the three neurotropic factors that reduce neural degeneration?

A
  1. apoptosis inhibitor protein
  2. brain derived neurotrophic factor
  3. glial-cell-line-derived factor
216
Q

what do the studies pertaining to introducing myelinated Schwann cell sheaths into damaged areas reveal?

A

can help a lot in rats who are paraplegic

217
Q

what do the studies on stem cells in regeneration show?

A

they do not replicate ad infinitum in principle, but we can induce them from skin cells, but the manipulation that is required to do so makes it difficult to guess how they would work.

218
Q

what are the largest effects of neuron neurotransplantation? (3)

A
  1. remyelination of injured axons
  2. releasing neurotrophic and guidance models
  3. developing into glial cells (not replacing dead or dying cells)
219
Q

what is constraint induced therapy?

A

tying down fully functional limbs to force intensive training of the other damaged limb in order to stimulate neural competition and advance its functional developmen

220
Q

what is the prevelaance of phantom limb?

A

most amputees, and 20% of those who are born without aa limb

221
Q

what its he percentage of those who experience painful phantom limbs?

A

50% of those who experience them in general

222
Q

what finding developed what method of treating phantom limb pain has been somewhat successful?

A

by finding where the brain has relocated the feedback that should be in their arm (ie, face).
this led to the belief that the pain was in the ‘mind’ lol, so they began to try to teach the people how to move their phantom limb by constructing aa feed back mechanism that showed them their good limb while they move their bad one, and after some time, pain subsides

Psych370 (37 decks)

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