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NEUR 1203 > Midterm - Review > Flashcards

Midterm - Review Flashcards

1
Q

Necrosis

A

Premature cell death where cells rupture, spilling their content into extracellular space

Results in inflammatory response

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2
Q

Apoptosis

A

Programmed cell death

Cells are dismantled into membrane-bound vesicles

‘Cell Suicide’

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3
Q

Traumatic Brain Injury

A

ABI which includes on damage to the brain caused by an external mechanical force

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4
Q

Cause of TBI

A

When a blow to the head is sufficiently forceful the CSF is unable to protect the brain resulting with a collision of the brain and skull

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5
Q

Coup TBI

A

Brain collides with skull on same side of impact

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6
Q

Contrecoup TBI

A

Brain collides with skull on opposite side of impact

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7
Q

TBI severity depends mostly on degree of _______

A

Rotational Force - skull rotates and brain is to slow to catch up

Can result in sheared corpus callosum or torn bridging veins

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8
Q

Site of Contact with skull in TBI

A

Swelling (edema) or Bleeding (hematome) which can lead to Intracranial Pressure (ICP)

Necrotic Death due to direct impat (causing cells to rupture)

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9
Q

Generalized Damage in TBI

A

Possible infection from penetration or open trauma

Diffuse injury throughout brain due to different density of white and gray matter

Diffuse Axonal Injury (DAI) - twisting and shearing forces cause axon to be torn from cell body (axotomy)

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10
Q

Energy Crisis faced in TBI

A

Disrupted blood flow leads to:

Lack of Oxygen (hypoxia) - causes switch to anaerobic metabolism which leads to overproduction of lactic acid (acidosis) which damages BBB

Lack of Glucose (Hypoglycemia) - leads to cognitive deficits and further reduction in ATP production

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11
Q

Excitotoxicity

A

Excess Glutamate

Glu continously binds to and activates post-synaptic receptors leading to Ca2+ influx, resulting in depolarization, Ca2+ get sequestered in Mitochondria which disrupts production of ATP

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12
Q

Causes of Excitotoxicity

A

TBI - Necrosis (Excess Glu due to rupturing cells)

Stroke - Neuronal Depolarization

HD & ALS - Decreased Glu reuptake

AD - Due to Atrophy

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13
Q

Immune Activation in TBI

A

Microglia secrete pro-inflammatory cytokines

Environmental stress increased toxic Reactive Oxygen Species (ROS) production which leads to Oxidative Stress

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14
Q

Oxidative Stress

A

Result of = ROS > AntiOX

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15
Q

Immune Privilege

A

Sites of body able to tolerate introduction of foreign substances without eliciting inflammatory response

Brain is NOT immune privileged due to interaction with peripheral immune system

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16
Q

Concussion

A

Mild TBI - a head injury with a temporary loss of brain function

  • Upper brainstem & RAS* - Alterations of consciousness
  • Corpus Callosum & Ant. Commissure* - Altered neurological function
  • Vascular Injuries* - Headache, dizziness, fatigue
  • Hippo. & Frontal Lobe* - memory, attention, concentration
  • Amyg. & Basal Forebrain* - mood and emotion
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17
Q

Chronic Traumatic Encephalopathy (CTE)

A

Progressive degenerative disease found in an individual with a history of multiple concussions

Brain Changes: Decreased brain weight, enlarged ventricles, neuronal death, tau aggregates, beta-amyloid plaques

Symptoms: Memory impairment, erratic behavior, impulsivity, depression, suicidal thoughts

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18
Q

Neurocirculation

A

Brain’s blood supply comes from Common Carotid and Vertebral Arteries (form Circle of Willis)

Main arteries which rise to brain - ACA, MCA, PCA

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19
Q

Stroke

A

Interruption of blood flow to the brain

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20
Q

Ischemic Stroke

A

Blockage in blood vessels

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21
Q

Ischemia

A

Lack of blood flow to tissue or organ

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22
Q

Hemorrhagic Stroke

A

Rupture in blood vessels

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23
Q

Ataxia

A

Reuslt of Cerebellar stroke

Motor impairments, difficulty walking, balance and coordination problems

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24
Q

Brain’s Energy Supply

A

Brain relies on blood supply to get Glucose and Oxygen (energy supply)

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25
Q

What causes a stroke?

A

Narrowing of arteries in neck or brain (cholesterol deposits)

Genetic mutations which increase risk of hypercholesterolemia, damage blood vessel walls, or cause clotting disorders

Environmental/Experiental factors which increase inflammation of vessel walls (High BP, smoking, obesity, alcoholism)

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26
Q

Intracerebral Hemorrhagic Stroke

A

Blood vessel ruptures

Blood leaks into surrounding brain tissue and creates swelling (edema) and ICP

Necrosis

Causes: High BP and aging blood vessels

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27
Q

Subarachnoid Hemorrhage

A

Bleeding in subarachnoid space

Cause: Brain Aneurysm (blood-filled bulge in weakened blood vessel wall)

Prognosis not good - 40-50% mortality rate

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28
Q

Transient Ischemic Attack (TIA)

A

Mild Ischemic Stroke (Mini Stroke)

Similar to stroke - only lasts minutes-hours

Leads to more severe attack 15-30% of time

Could be adaptive (prepares brain for more severe attack)

Treatment - Anti-coagulants (blood thinners)

29
Q

Core of Stroke

A

Area directly fed by occluded vessel

Less than 20% normal blood flow

Necrosis and Apoptosis

30
Q

Penumbra of Stroke

A

Outskirts of lesion, receive blood flow from other vessels

20-40% of normal blood flow

Apoptosis - Ripple Effect

31
Q

Stroke Necrosis

A

Lack of oxygen → switch to anaerobic glucose metabolism → Acidosis → decreased membrane permeability → Ions and water rush into cell → cells swell and rupture

32
Q

Stroke Apoptosis

A

Lack of Glucose → no fuel for Na/K pumps → Cells Depolarize → flooding of Glu leads cells to initiate self-destruct

33
Q

Damaged BBB in a Stroke

A

During Ischemia, epithelial cells are weakened (due to hypoxia and resulting acidosis) → during reperfusion peripheral immune cells can leak through and exacerbate immune response and inflammation

34
Q

Increase Ca2+ in Stroke

A

Result of Neuronal depolarization

Triggers release of Glu

Excess Calcium results in production of ROS - as a result Mitochondria can’t deal with stress and release signals to induce apoptosis

35
Q

Collateral Circulation

A

Blood flow through secondary pathways after the obstruction to the principle pathway occurs

36
Q

Neuroplasticity

A

Ability of the brain to reorganize and form new connections

37
Q

Neuroplasticity after a Stroke

A

Following neuronal death and removal of death tissue, nearby undamaged neurons can migrate to affected area and take over some lost functions

38
Q

Regrowth after a stroke

A

Endogenous Repair:

Axonal sprouting - new connections from surviving neurons

Angiogenesis - vascular growth, restores flow of nutrients to affected area

39
Q

DNA

A

Packaged into Chromosomes in the cell’s nucleus

Can be copied - which allows for cell division and reproduction

40
Q

Genes

A

Segments of DNA that code for the production of specific proteins

(Recipes for proteins)

41
Q

Chromatin

A

DNA + Histones

DNA gets wrapped around proteins called Histones

This controls activity - if a gene is needed DNA qill unfrul to expose segments of DNA that must be processed (to mRNA then to Protein)

42
Q

Alleles

A

Variants (alternative forms) of a gene

Dominant - only need one to produce a phenotype

Recessive - need two to produce a phenotype

43
Q

Epigenetics

A

Changes in gene expression related to experience

The environment can cause certain genes to be turned on or off by changing accessibility via epigenetic markers

Acetylation - On, loosen

Methylation - Off, tighten

44
Q

Huntington’s Disease

A

Neurodegenerative genetic disorder

Follows autosomal-dominant pattern of inheritance

HD Gene located in Chromosome 4

45
Q

Symptoms of HD

A

Motor - chorea, occular movements, clumsiness, dystonia, athetosis

Cognitive - restlessness, agitation, irritability, lack of concetration, memory problems

Emotional - depression, apathy, anti-social behaviors, aggression

46
Q

Dystonia

A

Persistent and intermittent muscle contractions causing abnormal and repetitive movements or postures

47
Q

HD symptoms later in disease

A

Bradykinesia, rigidity, difficult initiating and maintaining voluntary movement

Unable to function independently

Cognitive issues worsen - progressive dementia

48
Q

HD Prognosis

A

Death within 15-20 years of symptom onset

49
Q

Cause of HD

A

HD Gene codes for htt (huntingtin)

HD Gene has a section containing repeat of the codon CAG, when there are more than 40 repeats this results in mutant htt which leads to HD

CAG codes for AA Glutamine (Gln) - long stretches of Gln result in misfolding and toxic protein aggregates in cells

50
Q

HD Pathology cause

A

Increased mhtt function + Loss of WThtt function = HD pathology

51
Q

Where does neurodegeneration occur in HD?

A

Basal Ganglia: Striatum → Medium-Spiny Neurons (MSNs) of caudate nucleus and putamen

Cerebral Cortex → Pyramidal Projection Neurons + Neurons with projections to motor cortex and limbic structures

52
Q

Mutant htt in HD

A

Mutant htt accumulates in the nucleus of neurons (this is correlated with length of CAG repeats)

53
Q

How do mhtt aggregates form?

A

When mhtt is produced, cell knows this is an irregular protein and releases factors to cut these proteins and dispose → some fragments end up sticking together and creating protein aggregates

54
Q

GABA and HD

A

Upregulated in early stages, followed by marked reduction

Increased upregulated GABA activity + dysfunctional Glu activity in corticostriatal circuit → disruption of integrative processes by MSNs

GABA may initially by upregulated to deal with excess Glu

55
Q

Glutamate and HD

A

Evidence of excitotoxic neuronal death in HD brains

Increased Glu receptor stimulation → symptoms of HD

Excitotoxcity due to decreased reuptake of Glu

56
Q

Upper Motor Neurons

A

Originate in either the motor cortex or brainstem → axons extend to synapse onto LMNs

Bring motor commands to LMNs

May act directly or through interneurons

Release Glutamate

57
Q

Lower Motor Neurons

A

Originate in brainstem or spinal cord → axons leave CNS and synapse onto muscles

Receive signals from UMNs and bring messages to muscles

Can pass through spinal nervs (limbs and trunk) or cranial nerves (head and neck)

Release ACh at NMJ

58
Q

Corticospinal Tract

A

UMNs from motor cortex → Spinal Cord

Control muscles of limbs and trunk

Most axons decussate at medulla

59
Q

Corticobulbar Tract

A

UMNs from motor cortex → LMNs brainstem

Contols muscles of head and neck

Some decussate and some remain ipslilateral

60
Q

Upper Motor Neuron Damage

A

Failure to inhibit LMNs

Without inhibition LMN keeps telling muscles to contract → sustained contraction → stiffness and rigifity of muscles (spasticity) and hypertonia

Hyperreflexia - increase in muscle stretch reflexes

No muscular atrophy

61
Q

Damage to Lower Motor Neurons

A

Unable to tell muscle to start contracting

Result is no contraction of muscles → flaccidity, hypotonia, fasciculations (twitching)

Hyporeflexia - decrease in muscle stretch reflex

Muscle atrophy

62
Q

Amyotrophic Lateral Sclerosis

A

Degeneration of upper and lower motor neurons controlling voluntary movements

Use it or lose it → muscles that do not get ussed will atrophy (waste away)

Muscles are NOT dying first → wires connecting brain to muscle are degenerating and muscles are receiving signals

63
Q

ALS Symptoms

A

Weakness in arms (sporadic) and legs (familial) first

Eventually - loss of control of all voluntary muscles in arms, legs, trunk, neck, and head

64
Q

ALS prognosis

A

Fatal

3 years - 50%

5 years - 80%

only 10% live longer than 8 years

65
Q

Riluzole

A

Treatment for ALS which increases life expetancy 2-3 months

Slows loss of muscles by blocking sodium channels and decreasing glutamate

66
Q

LMNs and UMNs in ALS

A

LMN degeneration → muscle atrophy and fasciculations

UMN degeneration → spasms, increased muscle tone, abnormal reflexes

67
Q

Astrocytes in ALS

A

Release toxins which lead to motor neuronal death

Necroptosis (programmed necrosis)

68
Q

Glutamate and ALS

A

Decreased Glu transporters → Excitotoxicity

69
Q

Action Potential

A
  1. Depolarization

NEUR 1203 (9 decks)

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