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Mechanism of Disease > Exam 2: Common Neurological Disorders > Flashcards

Exam 2: Common Neurological Disorders Flashcards

1
Q

Nervous System

What is the structure of the CNS?

A

Brain and spinal cord
Overall “command center”
Processing and integrating information

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2
Q

Nervous System

What is the structure of the PNS?

A

Nerves and ganglia
Receives and projects information to and from the CNS
Mediates some reflexes

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3
Q

Nervous System

What is the function of the motor nervous system?

A

Some CNS and PNS components - includes all axons that transmit nerve impulses from the CNS to a muscle or gland
Somatic
Autonomic

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4
Q

Nervous System

Sensory Nervous System

A

Includes all axons that transmit impulses from a peripheral structure to the CNS (includes Eyes and Ears)
Somatic sensory
Visceral sensory

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5
Q

Special Senses: Glaucoma

Pathogenesis of Glaucoma

A

Increased intraocular pressure
blocks blood flow through intraocular vessels (in the uvea)
Reduced blood flow deprives retina of nutrients (atrophy of retinal layer)

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6
Q

Special Senses: Glaucoma

What causes increased intraocular pressure?

A

Increased production of vitreous humor
Decreased drainage of vitreous humor

Accumulation of vitreous humor

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7
Q

Special Senses: Glaucoma

What causes atrophy of retinal layer?

A

reduced blood flow deprives retina of nutrients

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8
Q

Special Senses: Glaucoma

What is the pathology of glaucoma?

A

Retinal Atrophy
* Disrupted nerve fiber layer (axon layer)
* Fewer cells in ganglion cell layer
* Damage to layer of rods and cones
* Overall thinning of retina

Plexiform laters are barely visible

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9
Q

Special Senses: Glaucoma

What are the clinical symptoms of Glaucoma?

A

Retinal damage - blurred vision, impaired dark adaptation
Corenal damage - halos around lights
Optic Nerve Atrophy

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10
Q

Special Senses: Ostosclerosis

Otosclerosis

A

Disease of the middle ear
Hardening of the tissue in the ear
May be asymptomatic
Genetic Component

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11
Q

Special Senses: Ostosclerosis

What causes ostosclerosis?

A

Bony growth around oval window
* failure of resorption results in excess bone
* Immobilizes stapes (prevent vibration transmission)

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12
Q
A
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13
Q

Special Senses: Ostosclerosis

What is the pathogenesis of Otosclerosis?

A

Starts with bone resorption
* uncoupling of resorption/deposition

Proceeds with fibrosis and vascularization of the temporal bone

Dense new bone replaces fibrotic tissue
* anchors the footplate of the stapes (cant vibrate againt oval window - deaf)

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14
Q

Special Senses

Tinnitus

A

disease of the inner ear
ringining, hissing, whistling, humming, and/or roaring in the ears

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15
Q

Special Senses: Tinnitus

Transient Tinnitus

A

not associated with disease
excessive stimulation of hair cells

Signalling hasnt stopped - usually goes away within a day or 2

Loud concert, club, loud party, etc.

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16
Q

Special Senses

Persistent Tinnitus

A

Associated with hearing loss
associated with cochlear dysfunction or cranical nerve VIII dysfunction
hair cell damage w/hearing loss

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16
Q

Diseases of the PNS

What are the types of PNS Diseases?

A

Neuromuscular
Myelin sheath

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17
Q

PNS: Neuromuscular disease

Neuromuscular junctions

A

Terminals of motor axons synapse with sarcolemma
Neurotransmitter is acetylcholine

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18
Q

PNS: Neuromuscular disease

Neurotransmitters

A

Can be excitatory or inhibitory
Usually amines, amino acids, or small peptides
Degraded in synaptic cleft, or taken up by endocytosis (prevent prolonged stimulation)
May act as paracrine hormones outside the nervous system

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19
Q

PNS: Neuromuscular disease

How does Myasthenia gravis affect neuromuscular junctions?

A

Autoantibodies bind ACh receptors

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20
Q

PNS: Neuromuscular disease

How does Botulism toxin affect neuromuscular junctions?

A

Directly effects ACh release

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21
Q

PNS: Neuromuscular disease

How does Lambert-Eaton Syndrome affect neuromuscular junctions?

A

Attacks voltage-gated Ca2+ channels

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22
Q

PNS: Neuromuscular disease: Myasthenia Gravis

Myasthenia Gravis

A

Antibody-mediated autoimmune disease
* Autoantibodies against ACh receptors (85% of patients)
* Induce aggregation and degredation of receptors (decreased number of receptors)

Reduced ACh receptors
* On post-synaptic membranes
* Reduced responsiveness to ACh - muscle weakness

Antibodies also interact with the thymus
* benign thymoma (10% of cases)
* Thymic Hyperplasia (30%)
* B-cell follicles in thymus

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23
Q

PNS: Neuromuscular disease: Myasthenia Gravis

What are the clinical symptoms of Myasthenia Gravis?

A

Fluctuating weakness
* Increases over the course of the day
* increass upon exertion
* decreased muscle responsiveness upon repeated stimulation
Involvement of extra-ocular muscles

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24
Q

PNS: Neuromuscular disease: Myasthenia Gravis

What is the treatment for Myasthenia Gravis?

A

Acetylcholinedterase inhibitors (ACh persists in synaptic cleft)
Immunosuppressive therapy (glucocorticoids) or Plasmapheresis
Thymectomy for patients with thymoma

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25
Q

PNS: Neuromuscular disease: Myelin Sheath Disease

Myelin Sheath

A

Layers of membrane surround an axon
In CNS, gives white matter its characteristic macroscopic appearance
Function: important for signal transmisison
Transmit signal through salatory conduction

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26
Q

PNS: Neuromuscular disease: Multiple Sclerosis

Multiple Sclerosis

A

Myelin Sheath Disease
Autoimmune demyelinating disorder - Both genetic and environmental components
Lesions in myelin sheath reduce nerve transmission efficiency
Relapsing episodes of neurologic deficits
Freqiency increases with time, while recovery decreases

Linked to MHC component (DR2)
Also IL-2/IL-7 receptors

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27
Q

PNS: Neuromuscular disease: Multiple Sclerosis

Describe the replasing episodes of multiple sclerosis

A

variable duration (weeks to years)
gradual, partial recovery
don’t have full recovery
episodes increase over time but recovery decreases

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28
Q

PNS: Neuromuscular disease: Multiple Sclerosis

Why is MS an autoimmune disease?

A

Immune response to components of the myelin sheath
Presence of chronic immune cells (especially T cells and macrophages) around myelin sheath plaques

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29
Q

PNS: Neuromuscular disease: Multiple Sclerosis

What is the immune response of MS?

A

T helper cells initiate immune response against myelin antigens
Cytokine release promotes macorphage and leukocyte infiltration
Macrophages and leukocytes release agents to damage invaders
agents damage myelin sheath indtead - b/c no invaders

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30
Q

PNS: Neuromuscular disease: Multiple Sclerosis

Describe the tissue damage in MS

A

Consistent with other immune diseases
Immune response itself produces tissue damage
Lesions are firmer than surround tissue (sclerosis)

Myelin is very soft - soft tissue gets replaces with harder tissue

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31
Q

PNS: Neuromuscular disease: Multiple Sclerosis

What are common signs and symptoms of MS?

A

Unilateral visual impairment
Brainstem involvement
Spinal cord lesions

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32
Q

PNS: Neuromuscular disease: Multiple Sclerosis

How is the brainstem involved in MS?

A

Cranial nerve signs
ataxia
nystagmus
internuclear opthalmoplegia

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33
Q

PNS: Neuromuscular disease: Multiple Sclerosis

What causes unilateral visual impairment?

A

Signal transmitted to axon as well
only one eye

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34
Q

PNS: Neuromuscular disease: Multiple Sclerosis

What causes/results from spinal cord lesions?

A

Cause: motor or sensory nerves (tingly)
Spasticity and loss of bladder control

Signal in spinal cord is slow/glitchy

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35
Q

Diseases of the CNS

Types of diseases of the CNS

A

Ethanol Toxicity
Cerebrovascular Disease
Prion Disease
Motor Neuron diseases (degenerative)
Degenerative Diseases
Dementia (degenerative)

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36
Q

Diseases of the CNS: Ethanol Toxicity

Toxic Nerve Damage

A

Cellular and tissue loss due to toxicity
Carbon monoxide
Methanol
Ethanol
Radiation

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37
Q

Diseases of the CNS: Ethanol Toxicity

Toxic Nerve Damage: Unique considerations in the CNS

A

Isolation (BBB) - only toxins that can cross the BBB get into the CNS
Meabolic needs
repair capacity

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38
Q

Diseases of the CNS: Ethanol Toxicity

Ethanol-induced toxicity

A

Acute abuse is generally reversible
Chronic alcohol abuse associated with metabolic disturbances as well

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39
Q

Diseases of the CNS: Ethanol Toxicity

What are the 3 mechanisms that cause CNS damage due to ethanol abuse?

A

Mostly associated with liver damage

Hepatic encephalopathy - damage secondary to liver
Thiamine deficiency
Ethanol toxicity

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40
Q

Diseases of the CNS: Ethanol Toxicity

Hepatic Encephalopathy

A

Glial response within the CNS (cerebral cortex and basal ganglia)
Elevated ammonia and pro-inflammatory cytokines
Astrocytes will be altered

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41
Q

Diseases of the CNS: Ethanol Toxicity

How are astrocytes altered in hepatic encephalopathy?

A

Enlarged nuclei
Minimal reactive cytoplasm

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42
Q

Diseases of the CNS: Ethanol Toxicity

Thiamine Deficiency

A

Can be malnutrition or malabsorption
Associated with chronic ethanol abuse

43
Q

Diseases of the CNS: Ethanol Toxicity

Acute Thiamine Deficiency

Wernicke Encephalopathy

A

Psychotic symptoms
opthalmoplegia
Reversible with thiamine supplementation

44
Q

Diseases of the CNS: Ethanol Toxicity

Chronic Thiamine Deficiency

Korsakoff Syndrome

A

Irreversible
Short term memory problems
Confabulation

Associated with lesions in the thalamus

45
Q

Diseases of the CNS: Ethanol Toxicity

What is the pathology of chronic thiamine deficiency?

A

Early - dilated capillaries with prominent endothelial cells
Hemorrhagic/necrotic foci in ventricular walls of brain
Eventual cyst formation

46
Q

Diseases of the CNS: Ethanol Toxicity

Ethanol Toxicity in CNS

A

Direct or secondary to malnutrition
Cerebellar dysfunction in 1% of chronic alcoholics

47
Q

Diseases of the CNS: Ethanol Toxicity

What causes cerebellar dysfunction in chronic alcoholics?

A

Atrophy and loss of granule cells (intaneurons that transmit to purkinje cells)
* excitatory signal from rest of nervous system
* Participate in processing visual and motor information, as well as learning and memory

48
Q

Diseases of the CNS: Ethanol Toxicity

What are the clinical symptoms of Ethanol Toxicity?

A

Truncal ataxia
Unsteady gate
Nystagmus

49
Q

Diseases of the CNS: Ethanol Toxicity

What is the treatment for ethanol toxicity?

A

Get alocohol intake under control

50
Q

Diseases of the CNS: Cerebrovascular Disease

Cerebral Edema

A

Accumulation of excess fluid within brain parenchyma

51
Q

Diseases of the CNS: Cerebrovascular Disease

What causes cerebral edema?

A

Excess fluid leakage from blood vessels, or CNS cellular damage

52
Q

Diseases of the CNS: Cerebrovascular Disease

What are the 2 pathways for cerebral edema?

A

Vasogenic - BBB disruption and increased vascular permeability allow fluid to move from within vasculature to within parenchymal space
Cytotoxic - Secondary to cell membrane injury (neuron, glia, endothelium)

53
Q

Diseases of the CNS: Cerebrovascular Disease

What causes cytotoxic cerebral edema?

A

Generalized hypoxia/ischemia
Metabolic disruption - ionic homeostasis

54
Q

Diseases of the CNS: Cerebrovascular Disease

What is the pathology of cerebral edema?

A

Gyro flattened/sulci narrowed
ventricles compressed
if untreated can result in herniation

55
Q

Diseases of the CNS: Cerebrovascular Disease

What are the clinical symptoms of cerebral edema?

A

Range from subtle neurological deficits to death

56
Q

Diseases of the CNS: Cerebrovascular Disease

Focal Cerebral Ischemia

A

Limited to no blood flow to a specific area of brain
Arterial occlusion or hypoperfusion

57
Q

Diseases of the CNS: Cerebrovascular Disease

What causes focal cerebral ischemia?

A

Embolism
Vascular inflammation (hyperperfusion)
In-situ thrombosis (atherosclerosis most frequently)

58
Q

Diseases of the CNS: Cerebrovascular Disease

What happens if focal cerebral ischemia is sustained?

A

Will develop cerebral infarct
Size/location dependent on vessels involved and duration

59
Q

Diseases of the CNS: Cerebrovascular Disease

What is the immune response to focal cerebral ischemia?

A
  1. neuronal stress (red neurons)
  2. Macrophages and reactive gliosis to clean up damage
  3. Repair - removal of tissue, loss of architechure, gliosis
60
Q

Diseases of the CNS: Prion Diseases: Creutzfeldt-Jakob

What are prions?

A

Abnormal forms of a cellular protein (specific protein called the Prion Protein (PrP)

61
Q

Diseases of the CNS: Prion Diseases: Creutzfeldt-Jakob

What do prions do?

A

Cause rapidly progressive neurodegenerative disorders:
* sporadic, familial or transmitted
* Creutzfeldt-Jakob disease, fatal familial insomnia, and kuru in humans
* Scrapie in sheep and goats
* Bovine spongiform encephalopathy (mad cow)

62
Q

Diseases of the CNS: Prion Diseases: Creutzfeldt-Jakob

What is the common pathology of prion diseases?

A

Spongiform change caused by intracellular vacuoles in neurons and glia

63
Q

Diseases of the CNS: Prion Diseases: Creutzfeldt-Jakob

What is the common clinical presentation of prion diseases?

A

rapidly progressive dementia

64
Q

Diseases of the CNS: Prion Diseases: Creutzfeldt-Jakob

How are prions formed?

A

PrP: 30 kD cytoplasmic protein present in neurons
Conformational change: from its normal alpha-helix containing isoform (PRPc) to an abnormal beta-pleated sheet isoform (PRPsc)

64
Q

Diseases of the CNS: Prion Diseases: Creutzfeldt-Jakob

Spongiform Changes in Prion Diseases

A

Cerebral cortex
Often, disease progresses so rapidly no noticeable atrophy is seen on gross examination of brain
Average survival is 7 months

65
Q

Diseases of the CNS: Prion Diseases: Creutzfeldt-Jakob

What are the symptoms of prion diseases?

A

Changes in memory/behavior
Dementia
Startle myoclonus

66
Q

Diseases of the CNS: Prion Diseases: Creutzfeldt-Jakob

Bovine Spongiform Encephalopathy

A

Variant of CJD (no alteration in PrP gene)
Caused by ingestion of prions from contaminated beef or blood transfusion
damage in the cerebral cortex

67
Q

Diseases of the CNS: Prion Diseases: Creutzfeldt-Jakob

Kuru Plauqes

A

Extracellular aggrgated PrPsc
Detectable with PAS or Congo red
Usually found in the cerebellum not in cerebrum
Also found inh vCJD

68
Q

Diseases of the CNS: Motor Neuron Diseases: ALS

Amyotrophic Lateral Sclerosis (ALD)

Lou Gehrig’s Disease

A

Motor Neuron Disease
Loss of lower motor neurons (spinal cord/brain stem)
Loss of upper motor neurons (project into spinal cord)
5-10% are familial (90-95% are sporadic)

69
Q

Diseases of the CNS: Motor Neuron Diseases: ALS

What is the amyotrophic portion of ALS?

A

Muscular paralysis with absence of atrophy
Also, hypertonia (rigidity) and exaggerated deep muscle tendon reflexes

70
Q

Diseases of the CNS: Motor Neuron Diseases: ALS

What is the lateral sclerosis portion of ALS?

A

Degeneration of corticospinal tracts
Produces upper and lower motor neuron paralysis in the extremities

71
Q

Diseases of the CNS: Motor Neuron Diseases: ALS

Familial ALS

A

25% are gain of function mutation in copper-zinx superoxide dismutase (SOD1)
Others:
* Dynactin (retrograde transport)
* VAMP-associated protein B (regulation of vesicle transport)
* Alsin (has guanine nucleotide exchange factor domains; regulates endosomal trafficking)

72
Q

Diseases of the CNS: Motor Neuron Diseases: ALS

SOD1 and ALS

A

Impaired ability to eliminated ROS originally thought to kill neurons
UPR induced by misfolded SOD1 is. now thought to be most likely mechanism
May also contribute to malfunction of glial cells

73
Q

Diseases of the CNS: Motor Neuron Diseases: ALS

ALS Pathogenesis

A

SOD1 mutation
Altered axonal transport
Neurofilament abnormailites
Glutamate toxicity (increases intracellular calcium)
Development of protein aggregates (bunina bodies, PAS-binding inclusions in the cytoplasm)

Possible mechanisms

74
Q
A
74
Q

Diseases of the CNS: Motor Neuron Diseases: ALS

Clinical Presentation of ALS

A

Loss of motor neurons/nerves
* hand weakness
* arm and leg spasiticity/cramping

Eventually
* Muscle strength and bulk decrease
* fasciculations

Death usually results from involvement of respiratory muscles (repeated infections)

75
Q

Diseases of the CNS: Degenerative Diseases: Parkinson’s

Parkinson’s disease

A

Degenerative disease
Degeneration of the substantia nigra (SN) in the basal ganglia
Tremor, rigidity, bradykinesia
L-DOPA responsive

76
Q

Diseases of the CNS: Degenerative Diseases: Parkinson’s

Parkinson’s like diseases

A

associated with toxin or other cause
e.g. a dopamine antagonist

77
Q

Diseases of the CNS: Degenerative Diseases: Parkinson’s

Parkinson’s Disease: SN pallor

A

Loss of pigmented neurons (B)
Associated gliosis

78
Q

Diseases of the CNS: Degenerative Diseases: Parkinson’s

Parkinson’s Disease: Degeneration of neurons

A

Lack of dopamine

79
Q

Diseases of the CNS: Degenerative Diseases: Parkinson’s

Parkinson’s Disease: Lewy Bodies

A

Eosinophilic cytoplasmic inclusions
alpha-synuclein fibers

80
Q

Diseases of the CNS: Degenerative Diseases: Parkinson’s

α-synuclein

A

Lipid-binding protein associated with synapses
mutation is associated with increased gene copy - gene dosage effect

81
Q

Diseases of the CNS: Degenerative Diseases: Parkinson’s

overexpression of α-synuclein…

A

induces lewy body formation in mice
inhibits melanin production in skin
Activates melanin production in neurons

PD suspectibbility linked to melanoma incidence

82
Q

Diseases of the CNS: Degenerative Diseases: Parkinson’s

Neuromelanin is linked to…

A

increased oxidative stress susceptibility in dopaminergic neurons

83
Q

Diseases of the CNS: Degenerative Diseases: Parkinson’s

Molecular genetics of Familial PD: Associated gain of function mutations

A

Leucine-rich repeat kinase 2 (LRRK2)
α-synuclein
DJ-1 (redox stress response)
PINK1 (kinase that regulates mitochondrial function)

84
Q

Diseases of the CNS: Degenerative Diseases: Parkinson’s

Molecular genetics of Familial PD: Associated loss of function mutations

A

Parkin (associated with juvenile form)

85
Q

Diseases of the CNS: Degenerative Diseases: Parkinson’s

What are the genetic suggested mechanisms of PD?

A

Stress response (UPR, ROS) - α-synuclein
Defective proteasome function - parkin
Altered mitochondrial function - DJ-1, PINK1

86
Q

Diseases of the CNS: Degenerative Diseases: Parkinson’s

Parkinsonian Disorder: MPTP

A

1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine
Byproduct of synthetic opioid production

Contaminanted street drugs

87
Q
A
87
Q

Diseases of the CNS: Degenerative Diseases: Parkinson’s

Parkinsonsian Disorder: MPTP: Mitochondrial toxin

A

Used to generate model systems for PD research
Selectively injures dopaminergic neurons:
* unknown mechanism for selectivity
* However, dopamine exposure can increase ROS, so cells may be more sensitive to mitohcondrial damage

88
Q

Diseases of the CNS: Degenerative Diseases: Parkinsonian Disorder

MPTP Mechanism of Action

A

Converted to N-methyl-4-phenylpyridinium (MPP+) in astrocytes
MPP+ inhibits complex I of the elctron transport chain
Reduced ATP production and oxygen metabolism
Increased ROS generation (Oxidative damage tolipids, proteins, nucleic acids

89
Q

Diseases of the CNS: Degenerative Diseases: Parkinsonian Disorder

What is the treatment for Parkinsonian Disorder: MPTP?

A

Remove exposure to toxin

90
Q

Diseases of the CNS: Dementia: Alzeherimer Disease

Dementia

A

Impairment of memory and other cortical function, while alertness is preserved

91
Q

Diseases of the CNS: Dementia: Alzeherimer Disease

Demetia: Alzheimer Disease

A

Most common cause of dementia (>50%)
5-10 year disease course
First sign is impaired learning and recall of recent memories

92
Q

Diseases of the CNS: Dementia: Alzeherimer Disease

What is the pathogensis of Alzheimer Disease?

A

Presence of specific amyloid plaques (extracellular, found in cerebral cortex and blood vessel walls(meningeal and cerebral))
Formation of neurofibrillary tanflws (NFTs)
Includes neuron and synaptic loss, as well as the presence of reactive astrocytosis and microglial proliferation

93
Q

Diseases of the CNS: Dementia: Alzeherimer Disease

Reactive astrocytosis

A

Increased size and number of astrocytes un response to traumatic injury
Synthesis and release of cytokines
Induce migration of immune cells into CNS
Astrocytes also remove excessive glutamate through specific transporters to prevent glutamate cytotoxicity

94
Q

Diseases of the CNS: Dementia: Alzeherimer Disease

Neurofibrillary tangles

A

No specific for AD
Paired helical filaments containing hyperphosphorylated tau
Also found in neuron processes (neurites) surrounding plaques

95
Q

Diseases of the CNS: Dementia: Alzeherimer Disease

Extracellular plaques

neuritic plaques

A

Central amyloid β core with ‘halo’
Surrounded by network of misshapen neuron processes
Microglia and reactive astrocytes at periphery (immune response)

96
Q

Diseases of the CNS: Dementia: Alzeherimer Disease

Proteins associated with AD: Presenilins

A

Subunits of γ-secretase
Important for proper amyloid processing, as well as other subtrates critical for neuron function

97
Q
A
98
Q

Diseases of the CNS: Dementia: Alzeherimer Disease

Proteins associated with AD: Apolipoprotein E4

A

Mediates LDL binding to receptor
Promoted Aβ formation and deposition, possibly through binding
ApoE3 binds tau (prevents aggregation?)

99
Q

Diseases of the CNS: Dementia: Alzeherimer Disease

Proteins associated with AD

A

Presenilins
Apolipoprotein E4
Amyloid β

100
Q

Diseases of the CNS: Dementia: Alzeherimer Disease

Aβ - induced neuronal damage

A

Directly cytotoxic
* number of plaques does not correlate well to disease

Synaptic dysfunction
* block long-term potentiation, other membrane changes

Inflammatory response
* mediators induce localized damage
* affect tau phosphorylation
* cause oxidative damage

101
Q

Diseases of the CNS: Dementia: Alzeherimer Disease

What are some consequences of neuronal loss?

A

Loss of:
Speech
Reading/writing
language comprehension

Mechanism of Disease (11 decks)

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