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Clinical Neuroscience > Unit 1 > Flashcards

Unit 1 Flashcards

1
Q

CNS

A

Central nervous system - spinal cord and brain

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2
Q

PNS

A

nerves and ganglia outside the brain and SC, including cranial nerves

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3
Q

Ramon y Cajal

A

Used the Golgi stain (which stains specific neurons entirely) to determine that the nervous system is contiguous

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4
Q

Cresyl Violet staining stains…

A

Cell bodies - nucleolus and ER

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5
Q

Groups of cell bodies in the CNS are called _____ while groups of cell bodies in the PNS are called _____

A

Nuclei ;ganglia

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6
Q

Layers of neuronal bodies are called ______

A

Laminae

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7
Q

Axons traveling together in the CNS are called _____ and in the PNS are called ______. Another name is ______

A

Tracts; nerves; fasciculi

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8
Q

What are the four main types of glia?

A

Astrocytes, Oligodendrocytes, Schwann cells, Microglial cells

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9
Q

Astrocytes function

A

Form the BBB, maintain the chemical environment around neurons, only in CNS

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10
Q

Oligodendrocytes function

A

Make myelin in the CNS

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11
Q

Schwann cells functions

A

Make myelin in the PNS - very important in the regeneration of PNS neurons - form a tube distal to lesion and provide growth signals for regenerating axon

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12
Q

Microglial cells functions

A

Hematopoietic cells and like macrophages - scavengers and secrete cytokines at site of injury, more microglia increase with injury!

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13
Q

How does information travel into and from the nervous system?

A
  1. Internal and external environment
  2. PNS - Sensory components (sensory ganglia and nerves and receptors)
  3. CNS (cerebrum, diencephalon, cerebellum, SC - analysis and integration of motor and sensory information)
  4. PNS - Motor components (visceral motor system - symp, parasymp, enteric; somatic motor system - motor nerves)
  5. Effectors: smooth, cardiac muscles and glands (if visceral motor system); skeletal (striated muscles (if somatic motor system)
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14
Q

Motors neurons are _____ while sensory neurons are _______.

A

Efferents; afferents

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15
Q

Three Motor Components of the Nervous System

A
  1. Somatic motor system (conscious motor control)
  2. Autonomic nervous system (visceral, unconscious functions)
  3. Enteric nervous system (part of ANS that control gastric motility and secretion = small ganglia and lots of neurons in the gut!)
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16
Q

Somatic vs Autonomic efferents

A

Somatic: direct connection to muscle
Autonomic: 2 neurons - pre and post ganglionic fibers

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17
Q

Parasympathetic vs Sympathetic Divisions

A

Parasymp: Long preganglionic, ACh, short postganglionic, ACh
Symp: short preganglionic, ACh, long postganglionic, NE

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18
Q

Synapse direction is usually

A

Anterograde - pre to post synaptic
Exceptions: cannabinoids and some neurotrophic factors

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19
Q

Sequence of events involved in transmission presynaptically

A
  1. AP
  2. VGCC
  3. Synaptic Fusion
  4. Vesicles released!
    - Astrocytes help take in excess NT in synaptic cleft!
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20
Q

____ is the major excitatory NT and _____ is the major inhibitory NT

A

Glutamate; GABA

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21
Q

Amino Acid NTs

A

Glutamate, GABA, Aspartate, Glycine

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22
Q

Amines

A

DA, NE, EP, 5HT, histamines

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23
Q

Two types of post synaptic receptors

A
  • Ionotropic
  • GPCRs
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24
Q

Ionotropic

A

Ion channels, much faster signals

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25
Q

GPCRs

A

Slower, large effects, NT binds and starts a cascade

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26
Q

Gs Cycle

A
  1. NE binds to GPCR
  2. Alpha subunit undergoes GDP hydrolysis into GTP via GEF proteins
  3. Alpha activate adenylyl cyclase which converts ATP into cAMP that acts on PKA
  4. GAP protein deactivates alpha which reassociates with beta/gamma dimer
  5. PKA gets dephosphated by phosphotase and phosphodiesterase
  6. cAMP becomes ATP in mitochondria
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27
Q

_______ and ________ NTs usually only have GPCSRs

A

Dopamine and NE

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28
Q

Aminergic NTs are made in ______ numbers of neurons but are distributed _____ in the brain

A

small; largely

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29
Q

Opiod peptides

A

Enkephalin, endorphins, and dynorphins

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30
Q

Overall process of neuropeptide synthesis

A

Pre-propeptides are made and then cleaved into several different peptides from one long protein precursor (propeptide)

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31
Q

What are two types of atypical neurotransmitters?

A

Endocannabinoids and NO (nitric oxide)

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32
Q

What makes atypical neurotransmitters atypical?

A

They are released retrogradely (post to pre) and they are calcium dependent
- both diffuse through membranes

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33
Q

Three classes of cell signaling molecules

A
  1. Cell impermeant - typical NTs
  2. Cell permeant - hormones, anandamide, and NO
  3. Cell associated - important in development
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34
Q

Activation of G-proteins

A
  1. Receptor binds to g-protein
  2. NT binds to receptor
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35
Q

Activation of G-proteins

A
  1. Receptor binds to g-protein
  2. NT binds to receptor
  3. Conformational change in receptor
  4. GDP comes off via GEFs, alpha subunit comes off and goes to inhibit/activate effector protein
  5. GAP binds GDP back to alpha
  6. Alpha associates with beta/gamma dimer
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36
Q

How g-protein signals terminate

A
  1. NT/Ligand dissociates from receptor
  2. Endocytosis of receptor (think LTD)
  3. GTP hydrolysis to GDP (GAP)
  4. Phosphodiesterases (PDE) converts cAMP to AMP which then turns into ATP
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37
Q

What are short term effects in a cell?

A

Protein function is changed

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38
Q

What are long term effects in a cell?

A

Gene expression, altered protein synthesis and expression!

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39
Q

Types and Functions of GPCRs

A
  1. Trimeric - most common
  2. Monomeric - growth factor receptors!
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40
Q

How are eukaryotic chromosomes packed?

A

Chromatin - DNA (negatively charged) plus histones (positively charged) plus other proteins that are important for DNA replication and gene expression

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41
Q

Pedigrees analysis

A

Show a family tree to determine whether a disease may be dominant, recessive, or x-related

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42
Q

Mitochondrial inheritance

A

Mother passes on to all her children

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43
Q

Autosomal dominant

A

Look for vertical inheritance - affected individuals in all generations

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44
Q

Autosomal recessive

A

Look for horizontal inheritance - parents without disease can have children with the disease

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45
Q

X-Linked recessive

A

Female carriers, males affected, daughters are affected only if father is affected and mother is a carrier

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46
Q

X-linked dominant

A

Both males and females are affected, affected father = only daughters are affected, affected mother = both daughters and sons are affected

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47
Q

Genetic vs epigenetic inheritence

A

Genetic: can’t change, inherited over generations
Epigenetic: modification of a nuclear gene in an organism - methylation, acetylation, X inactivation, environmental changes!

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48
Q

True or False: mutations happen due to pre-existing requisites

A

False, mutations are random, but can increase with mutagens

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49
Q

Types of mutations

A
  1. Gene mutations (nonsense, missense, frameshift, indel, TNREs)
  2. Chromosome mutations (large lengths of DNA - deletions, inversions, duplications, translocations)
  3. Chromosome numbers (CNV - copy number variants; aneuploids - incomplete sets or extra chromosomes)
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50
Q

Monogenic neurological diseases

A

Huntington’s, Fragile X, Rett Syndrome, Early onset AD

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51
Q

Polygenic diseases

A

Most diseases!
Depression, diabetes, heart diseases, epilepsy

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52
Q

What kind of studies allow for an estimation of heritability in humans??

A

Twin studies!

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53
Q

What are the three ways of protecting the brain

A
  1. BBB
  2. Ventricular system
  3. Cranial meningues
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54
Q

What is the BBB made from?

A

Capillary endothelial cells and tight junctions of astrocytes

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55
Q

What kind of drugs and molecules can get into the brain through the BBB?

A

Hydrophobic and non polar ones

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56
Q

What is in ventricles?

A

Cerebrospinal fluid

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57
Q

Where is CSF made?

A

Choroid plexus

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58
Q

What does CSF do?

A

Makes the brain boyuant

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59
Q

What are the three layers of the meningues?

A

Dura mater, arachnoid space, pia mater

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60
Q

What is in the subarachnoid space?

A

CSF!

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61
Q

Dura mater

A

2 layers, has pain receptors (trigeminal nerve!)

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62
Q

Arachnoid

A

Follows dura and doesn’t slip into sulci so there is subarachnoid space

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63
Q

Pia mater

A

Closely follows surface of brain and adheres to glia on brain

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64
Q

What is the main arterial pathway of blood supply to the brain?

A

Aorta –> common carotid artery –> internal carotid artery –> anterior/medial/posterior cerebral artery

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65
Q

What is the functions of the Circle of Willis?

A

Block of blood —> allows backup pathways of blood

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66
Q

Four parts of the spinal cord

A
  1. Cervical
  2. Thoracic
  3. Lumbar
  4. Sacral
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67
Q

Subparts of the brain

A
  1. Telencephalon
  2. Diencephalon
  3. Midbrain
  4. Cerebellum
  5. Pons
  6. Medulla
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68
Q

What are the 5 names of the brain regions?

A
  • Telencephalon - cerebrum
  • Diencephalon - thalamic structures
  • Mesencephalon - midbrain
  • Metencephalon - pons and cerebellum
  • Myelencephalon - medulla
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69
Q

Brain Imaging Techniques

A

CT
MRI
fMRI
PET
DTI

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70
Q

CT

A

X-rays make a 3D picture, structural

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71
Q

MRI

A

Grey matter structural images, magnetic field that responds to the spin of hydrogen atoms

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72
Q

DTI

A

Type of MRI for white matter

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73
Q

fMRI

A

Functional imaging, detects presence of oxygenated or deoxygenated protons (BOLD changes)

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74
Q

PET

A

Radioactive imaging - uses an isotope that can’t be metabolized which are more seen in active neurons

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75
Q

Stroke

A
  • cerebrovascular accident disruption of blood flow to brain
  • 3rd leading cause of death in US
  • learned anatomy stroke by stroke
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76
Q

A stroke is less that 24 hours it is…

A

TIA - transient ischemic attack

77
Q

A stroke is more than 24 hours it is…

A

a stroke - persistent focal sx

78
Q

Stroke Sx

A

Alteration in consciousness, headache, aphasia, facial weakness or asymmetry, incoordination, ataxia, visual loss

79
Q

FAST

A

Face, Arms, Speech, TIME

80
Q

Risk factors of stroke

A

Age, hypertension, heart disease, diabetes, smoking, alcohol, previous TIA or stroke

81
Q

Types of stroke

A

Ischemic and Hemmorhagic

82
Q

Which type of stroke is more common?

A

Ischemic

83
Q

What is ischemic stroke?

A

Insufficient blood supply - lack of oxygen and glucose to the brain

84
Q

What are the types of ischemic stroke?

A

Focal and global ischemic

85
Q

What is focal ischemic stroke?

A

Blockade of blood flow by a clot formed in the vessel (thrombotic) or an embolus made somewhere else (embolic)

86
Q

Global Ischemic Stroke

A

Global decrease in blood due to another event

87
Q

Thrombolytic cascade

A

Thrombin activates = converts fibrinogen into fibrin which cross links and forms a clot

88
Q

Pathways of making clots

A
  1. Extrinsic (damaged endothelial cells, bad cholesterol)
  2. Intrinsic (blood is exposed to collagen)
89
Q

Hemorrhagic stroke

A

Bleeding inside skull due to rupture of blood vessels or aneurysm –> bleeding into brain tissue!!!!

90
Q

Diagnosis of Stroke

A

Acute focal brain syndrome –> presists >24 hours —> CT high density (hemorrhagic) OR CT low density (ischemic - use MRI)

91
Q

What is another method to determine stroke?

A

Cerebral angiography - however, it can cause stroke and uses a dye that can cause allergy (insert dye into artery)

92
Q

Penumbra vs Core infarct

A

Penumbra - region surrounding core infarct region of stroke in which some blood flow remains and tissue is still viable and salvageable - seen in perfusion
Core- permanent destruction, seen in diffusion

93
Q

What is the goal when treating stroke?

A

To rescue penumbra tissue!

94
Q

What happens when blood flow stops in the core?

A

Necrosis - rapid cell death due to swelling and inflammation

95
Q

What happens when blood flow stops in penumbra?

A

Apoptosis - slow cell death - cytochrome c is released from the mitochondria and caspases are activation, leading to DNA fragmentation and cell shrinking (no inflammation)

96
Q

Loss of blood flow means…

A

Loss of glucose = loss of energy = no energy in cells to use Na/K ATPase = K levels outside rise and depolarize cell!

97
Q

Excitoxicity

A

The idea that a constant depolarization causes constant Ca2+ influx which leads to constant Glu release which leads to Ca+2 influx postsynaptically which triggers cell death (apoptosis - caspases due to cyt c release = DNA fragmentation)

98
Q

How do glia contribute to excitotoxicity?

A

Astrocytes use EAAT2 to reuptake glu, but that channel doesn’t work if the sodium gradient is disrupted - no reuptake = constant glu release and binding

99
Q

Glutamate is toxic to what other type of glia?

A

Oligodendrocytes

100
Q

Why is the brain so vulnerable?

A
  1. Needs a lot of energy but has no where to store it - relies on blood to bring glucose to make ATP
  2. No energy storage (no glycogen)
  3. Imperfect blood supply - ICA carries blood to entire brain while the MCA feeds many parts of the cortex
  4. Learning and stroke hing on the NMDA-R receptor - the cost of being smart is excitotoxicity!
101
Q

Treatment Options

A
  1. Restore blood flow by removing clot (tPA and mechanical removal)
  2. Restore and protect neurons (GABA increase, Glu decrease)
102
Q

How does tPA work?

A

tPA activated PLG that becomes plasmin, which breaks down fibrinogen and fibrin

103
Q

Downfalls of tPA

A
  • Only works within first 3 hours of sx onset
  • Giving to patients on anticoagulants
  • Giving to patients with bad blood pressure
104
Q

Neuroprotective treatments

A
  • NMDAR antagonists
  • Reduction of Ca2+ with blockers or calcium chelators
  • AMPA antagonists
  • Inhibitor of ROS
  • Hypothermia to reduce glu release and cell death
105
Q

Use of SSRIs in stroke

A

After a stroke, patients have increased plasticity - SSRIs can lengthen that plasticity window by reducing inhibitory activity so dendrites could resprout in affected areas – need to act fast after stroke though

106
Q

Components of brainstem

A

Midbrain, pons, medulla

107
Q

Midbrain components

A

Superior and inferior colliculi (sight and audio); substantia nigra (motor); PAG (pain), reticular formation (consciousness)

108
Q

Pons - What do they look like?

A

Stripy fibers, has parts of the reticular formation, large ventricle, descending motor neurons are ventral

109
Q

Medulla Oblongata components and functions

A

Vestibular control, reticular formation (heart rate and respiration), olives and pyramids (descending motor control)

110
Q

Difference between rostral and caudal reticular formation

A

Rostral - responsible for consciousness; regulate wakefulness and sleep-wake transitions
Caudal - Coordinates somatic and visceral motor neurons

111
Q

Internal structure of spinal cord

A

Gray matter = cell bodies, on the inside of the cord
White matter = axons, on the outside of the cord

112
Q

Lumbar vs Thoracic vs Cervical

A

Lumbar - Thickest gray matter
Thoracic - Grey matter is top heavy
Cervical - Grey matter is bottom heavy

113
Q

Touch Pathway

A

DRG cell bodies ipsilaterally all the way up to medulla (SYNAPSE and DECUSSATE) medulla to thalamus (SYNAPSE) thalamus to somatosensory cortex (SYNAPSE)

114
Q

Pain and Temperature pathway

A

Cell body in DRG to dorsal horn (SYNAPSE AND DECUSSATE) ascend contralaterally to medulla (SYNAPSE) medulla to cortex (SYNAPSE)

115
Q

What is the same about the pain and the touch pathways?

A

2nd neuron crosses the midline

116
Q

_____ information becomes lateral and ______ information becomes medial.

A

Dorsal; ventral

117
Q

Assessment of TBI can be done using the _____

A

Glasgow Coma Scale

118
Q

Range of Glasgow Coma Scale

A

3 - 15, lower = worse

119
Q

Damage to rostral brainstem symptoms

A

Limbs decorticate (lower limbs extend, upper limbs flex)

120
Q

Damage to caudal brainstem symptoms

A

Limbs decerebrate (all limbs extend - BAD because it may mean caudal reticular formation damage!)

121
Q

How does the CSF protect the CNS?

A

Buoyancy - reduces brain mass by a matter of 30
Injury often results in a coup-contre-coup movement

122
Q

TBI Types

A

Penetrating and non penetrating

123
Q

What happens in TBI?

A

Swelling of brain causes an increase of pressure, often due to leakage of blood which acts similar to a hemorrhagic stroke and lots of damage

124
Q

Damage at C5/C6

A

quadriplegic

125
Q

Damage in T or L regions

A

Paraplegic

126
Q

Damage in S regions

A

Loss of sensation in back of leg

127
Q

Damage caudal to medulla means

A

Ipsilateral touch and contralateral pain

128
Q

Damage rostral to medulla means

A

Contralateral pain and touch

129
Q

What happens most often in SCI?

A

Demyelination due to shearing

130
Q

True or false: TBI usually causes grey matter injury, while SCI causes white matter injury

A

TRUE

131
Q

Chronic Traumatic Encephalopathy (CTE)

A

Mild head injuries adding up, leading to dementia and have hallmarks of AD - tau fibrillary tangles and beta amyloid plaques

132
Q

Is there a causal link between the tau deposits and amyloid plaques?

A

NO

133
Q

What kind of cells get damaged in trauma

A

Vasculature, neurons, and glia

134
Q

What happens with the injury of vasculature and neurons?

A

Inflammation, glutamate excitotoxicity, axonal sprouting and demyelination (chronic - happens after trauma), all of which lead to cell death

135
Q

BBB damages causes

A

Excitotoxicity and fluid leakage

136
Q

PNS Regeneration

A
  • Regenerate really well
  • Proximal stumps form growth cones that grow along old path which is stimulated by diffusible factors secreted by Schwann cells and other organs
  • Synapses form back in original places
137
Q

CNS Regeneration

A
  • Not good
  • All types of glia are activated which seem to act as inhibitory signals to growing axons
  • Oligodendrocytes: make Nogo-A that binds to NgR1 on neurons which causes collapse of growth cones
  • Astrocytes: form glial scar and act as a physical barrier
  • Neurogenesis is very rare in CNS
  • Oligodendrocytes have multiple axons to bind to!
138
Q

Treatment of TBI

A
  • ABCs - airways, breathing, cardiac function
  • Imaging
  • Steriods and NSAIDs
  • Monitoring intracranial pressure
  • Anti-convulsants
  • Avoid fever (hypothermia)
  • Oligodendrocyte replacement
  • Rehabilitation
139
Q

Treatment of SCI

A
  • Same as TBI
  • Could also use GABA agonists for spasticity due to UMN damage so there may be a lot of contractions
  • Rehabilitation
140
Q

Clinical Trials for TBI and SCI

A
  • NMDAR antagonists to prevent excitoxicity
  • Masking NogoA
  • Blocking rho A (collapse of growth cones)
  • NSAIDs and levels rho decrease
  • Stem cells (including bone marrow and olfactory epithelial cells)
  • Estrogen (more SCI in men)
  • Robotic rehabilitation
141
Q

Differences between active transporters and ion channels

A

Active transporters: move selected ions against concentration gradient with the use of energy
Ion channels: ions diffuse down concentration gradient and are selectively permeable to certain ions

142
Q

What is the role of Na/K ATPase pumps?

A

Use the energy of ATP to pump K into the cell and Na out of the cell

143
Q

What happens to the Na/K ATPase when [ATP] decreases?

A

Less Na outside the cell, less K inside the cell = depolarization

144
Q

What do exchanger sand co-transporters use as energy?

A

Gradients of ions

145
Q

Types of Ion Channels

A
  1. Voltage-gated channels
  2. Ligand gated channels
  3. ASICs (activated by heat, pain, and temp)
  4. Mechanically activated channels
146
Q

How are synaptic potentials encoded?

A

By amplitude - higher amplitude means larger EPSP

147
Q

How are action potentials encoded?

A

By frequency - more APs means more active neuron

148
Q

What does the electrochemical equilibrium rely on?

A

Probability of an ion encountering a channel and going through it

149
Q

Nerst equation

A

58/Z (charge of ion) log(xout/xin)

150
Q

Membrane potentials summary

A
  1. Neuronal membranes tend to have resting potentials of -50 to -70 mV
  2. Resting membrane potential depends up the concentration gradients of the ions and the permeability of the membrane to K (at rest K channels are open)
  3. Hyperpolarize means membrane potential is more negative, depolarize means membrane potential is more positive
  4. When ions move across the membrane to affect the membrane potential, usually only a few ions are involved and the overall cellular concentrations of ions are relatively unchanged
151
Q

Action potential phases

A
  1. Resting potential: maintained by Na/K ATPase and K+ leak current
  2. Depolarization to threshold and Na+ channels open - Na+ rush into cell and depolarize the cell
  3. Repolarization: K+ channels open, sodium channels inactivate, K+ rushes outside, membrane potential hyperpolarized back to resting
  4. Hyperpolarization: can get overshoot
  5. Refractory period: Na+ channel still inactivated and cell is hyperpolarized
152
Q

Current flow of a particular ion is a combination of…

A

conductance (how open the channel is) and how far the membrane is from equilibrium potential of that ion

153
Q

Why don’t Na and K voltage gated channels open at the same time?

A

Na+ open immediately, but K+ open more slowly and Na+ channels inactivate with prolonged depolarization (when K+ channels open)

154
Q

True or false: APs can happen at any depolarization

A

False, they are only generated when a cell membrane is depolarized to a threshold

155
Q

EPSP vs IPSP

A

Excitatory vs inhibitory post-synaptic potentials - can summate in order to reach threshold (or prevent threshold!)

156
Q

Why do APs need passive conductance?

A

Passive conductance leads to decay over distances, but as long as sufficient depolarization reaches a voltage Na+ channel, the AP will continue!

157
Q

Myelin’s role in APs

A

Think of this as the insulation of a wire; AP travels by saltatory conduction because ions can’t leak out of myelin = increases passive conductance = ensures enough depolarization reaches the next node!

158
Q

What happens when axons are demyelinated?

A

Membrane is leaky = APs can’t keep going because there is not enough depolarization to reach threshold at the next path of Na+ channels

159
Q

Channelopathies

A

Mutations in ion channels

160
Q

AP reaches presynaptic terminal - now what?

A

VGCC open, let calcium in, vesicles fuse and Nt gets released

161
Q

Relationship between AMPA and NMDA receptors

A

Both are ionotropic glutamate receptors; AMPA opns faster, allowing Na+ influx which depolarizes the membrane. This causes the Mg2+ plug to be released from the NMDA channel and then NMDA receptors allow Na+ and Ca2+ to flow = important for plasticity and learning!

162
Q

GABA

A

an inhibitory NT

163
Q

Drugs that act on GABAa channels

A
  1. Barbiturates (agonists)
  2. Benzodiazepines (positive allosteric regulator = safer bc it needs GABA to work with it)
  3. Alcohol (facilitates GABA’s ability to open channels)
  4. Anesthetics (prolong GABAa channel opening)
  5. Antagonists (CAUSE seizures E:I ratio)
164
Q

GAT

A

Mops up excess GABA from a synapse

165
Q

Seizures

A

Uncontrolled synchronous firing of neurons in brain that cause behavioral abnormalities

166
Q

Epilepsy

A

Clinical syndrome with recurrent and spontaneous unpredictable seizures (chronic seizures for no reason)

167
Q

How is epilepsy diagnosed?

A

EEG - 21 electrodes placed in a defined pattern; summation of 100s of neurons firing (looking at synchrony of neurons firing)

168
Q

Ictal

A

seizure

169
Q

Interictal

A

between seizures

170
Q

Normal EEG

A

EEG activity is low

171
Q

EEGs during a seizure

A

Bigger, more synchronous rhythmic activity of neurons that correlates with behavioral effects

172
Q

MRI and CT in seizures

A

Can be used to find the location of a scar or damaged brain tissue

173
Q

MTLE

A

Medial Temporal Lobe Epilepsy; most common type of epilepsy that causes hippocampal damage (hippocampus has a sepcific pattern of firing and in epilepsy this pattern can get stuck)

174
Q

Types of seizures

A

Generalized - across both hemispheres
Focal - Small part of the brain, but can become a generalized seizure

175
Q

Generalized seizures types

A
  • Tonic clonic: rigidity (tonic) then twitching (clonic)
  • Absence: non-convulsive, brief loss of consciousness (Ca2+ channel blockers)
  • Myoclonic: Twitching or jerking due to motor cortex
  • Atonic seizure: loss of muscle tone
176
Q

Focal seizures types

A
  • Simple: short lasting seizures without loss of consciousness
  • Complex: impairment of consciousness
177
Q

Status epilepticus

A

Frequent, long lasting seizures without regaining consciousness between seizures

178
Q

Causes of seizures

A
  • Stress
  • Lack of sleep
  • Flashes of lights or sounds
  • Low blood sugar
  • Fever
  • Alcohol withdrawal
  • Hormones
  • Hyperventilation
179
Q

Why are babies more prone to seizures?

A

Direction of Cl- transport makes GABA either excitatory or inhibitory. In children GABA is excitatory and depolarizes through the NKCC1 receptor = more E = seizures are more often

180
Q

Genetics and epilepsy

A

50% of epilepsy, especially in children is caused by genetic disposition (usually channelopathies)

181
Q

Acquired Epilepsy

A
  • Most common in adults
  • Head injuries
  • Brain tumors
  • Stroke
  • Pre-natal
  • Infection
  • Vascular abnormalities
  • Autism
  • Febrile seizures
  • Mild TBI
  • Drugs
  • Sleep deprivation
182
Q

Epileptogenesis

A

things that may change the E:I ratio, thus leading to seizures
- Increased glu, decreased GABA
- Receptor, dendrite, synapse, astrocytes, ion transporter, signal changes

183
Q

Pyramidal cells and epilepsy

A

Cortical pyramidal cells fire at once due to gap junction coupling

184
Q

Basket cells

A

Interneurons that usually synapse on multiple pyramidal cells so that an individual interneuron can control the firing of many pyramidal neurons

185
Q

More inhibition from basket cells leads to ____ excitation

A

Less

186
Q

What can a mutation in a basket cell lead to?

A

Affects E/I balance

187
Q

Plasticity and epilepsy

A

Seizures can cause plasticity, so plasticity and neurogenesis is not helpful

188
Q

Treatment of Epilepsy - Drugs

A

Attempt to enhance GABA action or block Na+/Ca2+ (like barbiturates and benodiazepines)
- Valproate (blocks Na an dCa2+ and increases GABA)
- Topiramate (same as above)
- SSRIs (plasticity?)
- CBD

189
Q

Treatment of Epilepsy - Surgery

A

Temporal lobe surgery, corpus callosotomy (split brain), and hemispherectomy

Clinical Neuroscience (4 decks)

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