Neurological Disorders (Exam 1) Flashcards
1
Q
Three functions of the nervous system
A
Detect, analyze and transmit information
2
Q
Communicate through electrochemical signals
A
Neurons
3
Q
Somatic and autonomic
A
Peripheral nervous system
4
Q
Voluntary movement
A
Somatic
5
Q
Involuntary movement (parasympathetic and sympathetic)
A
Autonomic
6
Q
Arrive at CNS
A
Afferent
7
Q
Exit from CNS (brain and spinal cord)
A
Efferent
8
Q
Neurons do not
A
Divide
9
Q
Sensory receptor cells to the brain
A
Sensory neurons
10
Q
Brain to muscles
A
Motor neurons
11
Q
Info between neurons
A
Interneurons
12
Q
Modulate and regulate the electrical activity of a given neuron
A
Neurotransmitter
13
Q
Electrical signal that travels down the axon and is created using NA and inhibited by K
A
Action potential
14
Q
Three basic parts of a neuron
A
Soma, branching dendrites and axon
15
Q
Junction between two neurons; passes info between them
A
Synapse
16
Q
Open sodium and calcium channels leads to an action potential
A
Excitatory neurotransmitter
17
Q
Open chloride channels > hyper polarization > resting potential
A
Inhibitory neurotransmitter
18
Q
Resting potential average
A
-70 mV
19
Q
Barrier between circulation and the brain (exception: olfactory lobes)
A
Blood brain barrier
20
Q
Tight junctions from barriers
A
Endothelial cells
21
Q
Structural support, immune properties
A
Pericytes
22
Q
Structural support, recruits WBCs
A
Astrocytes
23
Q
The BBB is a highly
A
Selective semipermeable membrane
24
Q
Role of p-glycoprotein pumps
A
Remove harmful compounds
25
Lacks a functioning BBB; contains receptors to detect toxic substances that lead to emesis
Chemoreceptor trigger zone
26
Dysfunction of the BBB can lead to
Alzheimer’s or Parkinson’s
27
Most drugs are transported over the BBB via
Passive diffusion
28
Endogenous substances and amino acid derived drugs cross the BBB via
Carrier mediated
29
Endogenous substances such as hormones and LDL pass the BBB via
Receptor mediated
30
Some proteins pass the BBB via
Absorptive transcytosis
31
Substances pumped out of the BBB via
Active efflux
32
When a neurotransmitter also functions as a hormone
Neurohormones
33
When a neurotransmitter also functions as a hormone
Neurohormones
34
Membrane potential becomes more positive
Excitatory post synaptic potentials
35
Membrane potential becomes more negative
Inhibitory post synaptic potential
36
Depolarization approximately to
+35 mV
37
When potassium gates close slowly
Hyper polarization
38
When sodium channels close and potassium channels open, potassium flows out
Repolarization
39
Dopamine, norepinephrine and epinepherine
Catecholamines
40
Serotonin, dopamine, norepinephrine and epinephrine
Monoamines
41
Unpleasant sensory and emotional experience associated with actual or potential tissue damage
Pain (physiological)
42
Short duration and resolves
Acute
43
Longer than expected of healing; no useful physiological purpose
Chronic (pathophysiological pain)
44
How many people experience chronic pain at some point in their life?
1 in 3
45
From tissue damage due to trauma/inflammation; mechanical/temp/chemical stimuli
Nociceptive pain
46
Pain from musculoskeletal system (skin, bones, muscle, connective tissue)
Somatic
47
Pain from visceral organs (abdominal pain)
Visceral pain
48
Cancer can be from what type of pain
ALL TYPES OF PAIN :(
49
Functional pain
pain with no identified origin
50
Physiology of Pain (5 steps)
1. transduction
2. conduction
3. transmission
4. modulation
5. perception
51
1. Transduction (Pain process)
sensory neurons activated to noxious stimuli
52
2. Conduction (Pain process)
action potential travels along the neuron to the spinal cord (A fibers and C fibers)
53
what are A fibers? what are C fibers?
A fibers - myelinated neurons; first pain
C fibers - unmyelinated fibers; 2nd pain
54
3. Transmission (pain process)
sensory neurons release substances that activate a 2nd neuron in spinal cord and sends a message to the brain
55
4. Modulation (pain process)
pain can be facilitated or inhibited depending on which substances are released
56
5. Perception
complex interaction between ascending and descending pathways and various brain systems
57
overtime pain pathways become
stronger with repeated pain and leads to pain hypersensitivity
58
allodynia
pain caused by stimulus that does not normally provoke pain
59
hyperalgesia
increased response to stimulus that is normally painful
60
Substances that facilitate pain (3)
1. Substance P
2. Glutamate
3. Inflammatory mediators
61
substances that reduce pain (4)
1. endogenous opioids
2. endogenous cannabinoids
3. GABA
4. serotonin and norepinephrine
62
Primary headache disorders
not due to another cause
63
primary headache examples (3)
1. tension
2. migraine
3. cluster
64
secondary headaches
due to another medical condition
65
secondary headache examples (3)
1. sinus headache
2. brain tumor
3. meningitis
66
migraine
moderate to severe headache interferes with normal functioning
67
how long do migraines last?
4-72 hours
68
two types of migraines
aura (25%)
without aura (75%)
69
aura
neurological symptoms that occur prior to and during a migraine headache; caused by cortical spreading depression
70
non rapid eye movement
not deep sleep, normal muscle tones, dec metabolism, HR,RR,BP
71
rapid eye movement
deep sleep and vivid dreams; inc in metabolism, low muscle tone, variations in VS
72
insomnia
difficulty falling asleep; constant awakening
73
the difference between primary insomnia and secondary insomnia
primary - unknown cause; 10-20%
secondary - stress; 80-90%
74
two types of sleep problems (insomnia types)
1. onset insomnia (initiating sleep)
2. maintenance insomnia (staying asleep)
75
Narcolepsy
uncontrollable excessive daytime sleepiness; altered REM/NREM
76
narcolepsy type 1
narcolepsy with cataplexy
77
cataplexy
loss of muscle control from strong emotions
78
narcolepsy part 2
narcolepsy without cataplexy
79
pathophysiology of narcolepsy
loss of orexin containing neurons
80
restless leg syndrome
desire to move limbs during rest
81
pathophysiology of restless leg syndrome
iron deficiency, poor circulation, dysfunction of dopaminergic neurotransmission
82
sleep apnea
repetitive upper airway, closure during sleep, decrease or stops in airflow leads to waking up
83
pathophysiology of sleep apnea
structure in jaw/neck or fatty deposits in neck
84
parasomnias
undesirable physical/behavioral phenomena occurs during sleep
85
NREM disorders of parasomnias
sleepwalking, sleep terrors, sleep talking, etc.
86
REM behavioral disorders
paralysis fails to occur during REM sleep, acting out in their dreams
87
circadian rhythms disorders
misalignment in sleep cycle
88
Guillain Barre Syndrome (GBS)
autoimmune disorder, attacks myelin around PNS neurons leading to schwann cell and neuronal damage
89
what is GBS triggered by?
infection or vaccine. it is typically reversible
90
symptoms of Guillain Barre Syndrome
-tingling sensation in extremities (paresthesia)
-difficulty with eye muscles, vision, swallowing, speaking, chewing
-pins and needles in hands/feet
-severe pain at night
91
Pathogenesis of GBS
molecular mimicry between offending agents and peripheral nerve gangliosides; leads to antiganglioside antibodies
92
Multiple Sclerosis
autoimmune, neurodegenerative disorder; attacks myelin surrounding CNS neurons leads to oligodendrocyte and neuronal damage
93
symptoms of MS are dependent
on location of demylenation
94
symptoms of MS in cerebellum
different in balance and coordination
95
symptoms of MS in optic nerve
loss of vision, eye pain, involuntary eye movements (nystagmus)
96
pathophysiology Outside In for MS
trigger activates T cell/B cell outside (PNS) and leads to infiltration of these cells into the CNS via dysfunctional BBB
97
pathophysiology Inside Out for MS
disturbance in a metabolic process in the brain, leading to release of inflammatory cytokines/chemokines which compromises the integrity of BBB allowing T and B cells in
98
Symptoms of MS occur based on
plaques
99
CIS
clinically isolated syndrome of MS; symptoms last 24 hours and may or may not be MS
100
RR
relapse remitting MS
101
PP
primary progressive MS
102
SP
secondary progressive MS
103
85% originally diagnosed with this type of MS
relapse remitting
104
Parkinson's disease
movement disorder which occurs due to loss of dopamine producing neurons in the substantia nigra; lewy bodies present
105
non motor symptoms of Parkinsons
Inosmia , rapid eye movement disorder, dementia, altered ANS function and REM sleep disorder
106
pathophysiology of Parkinson's
presence of Lewy bodies - abnormal aggregates of alpha synuclein protein in neurons - Lewy bodies in brain stem
loss of dopamine containing substantia nigra neurons lead to depigmentation in sub. nigra leads to motor symptoms
107
dementia
collection of symptoms including decline in memory, reasoning and communication skills
108
Alzheimer's
build up of beta amyloid plaques and neurofibrillary tangles
109
vascular dementia
damage to cerebral vasculation from conditions like hypertension, smoking, etc.
110
lewy body
Abnormal aggregates of alpha-synuclein protein which form inside of neurons
111
initial symptoms of lewy bodies
REM, hallucinations, etc.
112
Frontotemporal Dementia (Pick's Disease)
degeneration in frontal/ temporal lobes and abnormal tau accumulation
113
initial symptoms of Pick's disease
changes in personality, difficulty to produce language
114
glutamate is
excitatory, tells the neuron to fire
115
GABA is
inhibitory, dampens the firing rate
116
Who brings information to the cell body? who takes information away?
dendrite bring
axons take away
117
Neurotransmitter synthesis enzymes
enzymes responsible for the synthesis of the NT
118
VG Na+ channel
responsible for depolarization in neuronal action potential
119
VG Ca2+ channel
activated by membrane depolarization, CA influx leads to NT release
120
Postsynaptic receptors
activation of these receptors leads to the physiological response of the NT
121
Degrading enzymes
responsible for degradation of NT, can be located intra/extracellularly
122
reuptake pump/transporter
transporters responsible for uptake of the NT from the synapse back into the presynaptic neuron
123
Presynaptic autoreceptors
activation of presynaptic autoreceptors decreases NT release; negative feedback
124
vesicular transporter
located presynaptically and responsible for uptake of NT into vesicles for storage
125
Pathophysiology of circadian rhythm disorders
Misalignment of light-dark cycle of sleep
126
Oligodendrocytes
Myelinating neuronal axons in CNS
127
Schwann cells are the myelinating cells of the
PNS
128
Myelin
Fatty substance that increases the rate of action potential; protective layer
129
Nodes of Ranvier
Spaces between myelin sheaths with high density of VG NA channels; allows action potential to travel quickly
130
GBS attacks what type of neurons leading to what type of damage?
PNS neurons; Schwann cell and neuronal damage
131
Pathogenesis of Acute Inflammatory Demyelinating Polyneuropathy
Because of T cell mediated cytokine storm; no detectable antibodies
132
Acute Motor Axonal Neuropathy and Acute Motor and Sensory Axonal Neuropathy are associated with
Traditional anti ganglioside antibodies
133
In MS what type of neurons are attacked?
CNS neurons
134
What is the immune response when T cells encounter myelin in MS?
What do B cells produce?
Production of pro inflammatory cytokines, tumor necrosis factor alpha, interferon gamma
B cells produce auto antibodies
135
In MS, regulatory cells may
Reduce the immune response leading to periods of remission
136
MS plaques in brain stem lead to
Difficulty swallowing, slurred speech
137
MS plaques in the cerebellum lead to
Difficulty with balance and coordination
138
MS plaques around the optic nerve lead to
Loss of vision, involuntary eye movements (nystagmus)
139
MS plaques along the motor pathways lead to
Tremor, muscle weakness, muscle spasm, paralysis
140
MS plaques in sensory pathways lead to
Paresthesia, loss of sensation
141
MS plaques in the cerebral cortex lead to
Cognitive impairment, fatigue
142
MS plaques on spinal nerves may result in
Urinary incontinence, sexual dysfunction and spasticity
143
Parkinson’s diseases may be ___ or ___
Familial or sporadic
144
Most of the medications used in PD
Enhance dopamine this neurotransmission but does NOT reduce or prevent loss of neurons
145
Essential criteria for diagnosis of PD
Bradykinesia with at rest tremor and rigidity
146
PD is characterized by
Lewy bodies in the brain stem
147
Alpha- synuclein
Endogenous protein found in presynaptic nerve terminals
148
Reduction in dopamine in what pathway leads to motor symptoms of PD?
Nigrostriatal pathway
149
Bradykinesia?
Dyskinesia/hyperkinesia?
Too little dopamine
Too much dopamine
150
Lewy body dementia
Build up of alpha synuclein in the cortex
151
changes in the brain can
occur long before symptoms start to show
152
dementia is caused by ___ and nerve cells become ____ and certain parts of the brain ____.
1. physical brain diseases
2. damaged and start to die
3. starts to shrink
153
Amyloid plaques pathophysiology in AD
extracellular beta amyloid deposition leads to generation of senile plaques
154
Tau pathophysiology in AD
Tau becomes abnormally phosphorylated by kinases which leads to aggregation and structural dysfunction of neurons
155
Hyperphosphorylated tau
dissembles microtubules and damages the cytoskeleton and signal transduction processes of neurons
156
Other factors that play a role in AD (4)
neuroinflammation
cholinergic insufficiency
mitochondrial dysfunction
autophagy dysfunction
157
Alzheimers disease is a
neurodegenerative disorder
158
early onset AD
due to familial AD
due to mutations that lead to increased pathogenic amyloid beta
5% of cases
159
late onset AD
combination of genetic and environmental factors
95% of cases
160
genetic risk factor of Late onset AD
APOE4 gene
161
Cholinergic hypothesis of AD
loss of cholenerigc activity is associated with AD severity, enhancing cholinergic signaling preserves cognitive function (ex: inhibit AChE)
162
Glutamatergic hypothesis of AD
excess activation of NMDARs by glutamate leads to exitotoxicity and neuronal death in AD (block NMDARs to dec exitotoxicity)
163
Amyloid precursor protein
transmembrane protein that plays a role in neuronal growth and repair; cleaved by secreatases which leads to AD
164
Tau
intracellular protein that usually stabilizes neuronal microtubules
165
Preclinical AD
no symptoms but biomarker evidence, can be 20 years before presence
166
MCI due to AD
mild cognitive impairment; mild symptoms and biomarker
167
Dementia due to AD
impaired daily function and biomarker
168
examples of biomarkers (3)
decreased CSF AB42, increased CSF p-tau, decreased brain glucose metabolism
169
Diagnosis of AD is based on
clinical assesment
170
what is needed for a definitive diagnosis of AD
Histopathological analysis; done during autopsy
171
Image studies to support diagnosis of AD (3)
1. MRI - hippocamal atrophy
2. FDG-PET and SPET - reduced cerebral flow and metabolic changes
3. Amyloid PET - beta amyloid plaque density
172
convulsion
sudden attack of involuntary muscular contractions/relaxtations
173
seizure
abnormal CNS electrical activity
174
epilepsy
a group of recurrent disorders of cerebral function characterized by both seizures and convulsions
175
electroencephalogram
plays a central role in diagnosis with seizure disorders; can show irregular activity in the brain that indicates seizures
176
causes of epilepsy (7)
genetic, vascular, severe head trauma, infections, tumor, drug abuse, unknown
177
greatest cause of epilepsy
UNKNOWN!
178
Partial seizures and 2 types
excessive electrical activity in one cerebral hemisphere
types: simple and complex
179
Simple partial
preservation of consiouness
180
complex partial
loss of awareness at seizure onset, originate in frontal or temporal lobes
181
generalized seizures
excessive electrical activity in both cerebral hemispheres; loss of consciousness is common
182
generalized seizures originate in the ___
thalamus and brainstem
183
tonic seizures
sudden stiffening of the body, arms and legs
184
clonic seizures
rhythmic jerking movements of the arms and legs without a tonic component
185
does a normal of EEG rule out a seizure? why?
it does not rule out epilepsy. it can only show wavelengths during the test and the abnormal brain waves only happen during a seizure
186
other techniques that can help diagnose epilepsy
MRI
187
epilepsy
two or more unprovoked seizures that can't be explained by a medical condition
188
seizures are due to
an imbalance in excitation and inhibition in the brain
189
pathophysiology of epilepsy
neuronal networks are overreactive
can be enhanced excitatory (inc in glutamate)
can be reduced inhibitory ( dec in GABA)
can be enhancement of overall NT (inc in AP)
190
Brain injury
alterations in level of consciousness and in cognitive, motor or sensory function
191
focal brain injury
injury to one specific area
192
global brain injury
injury to entire brain or numerous areas of it
193
mechanisms of brain injury (4)
direct damage
ischemia/hypoxia
excitotoxicity
excessive intracranial pressure
194
excitotoxicity
due to glutamate buildup and excessive Ca2+ influx through NMDARs
195
Traumatic brain injury is the
leading cause of death and disability among people under than 24
196
primary injury of traumatic brain
damage caused by impact
197
secondary injury of traumatic brain
damage caused by subsequent brain swelling, infection or ischemia
198
concussion
mild type of TBI
199
persistent vegetative state
loss of all cognitive functions and awareness for at least one month
200
brain death
irreversible loss of function of the brain and brain stem
201
Psychological disorders
disturbances in mood, thoughts and behaviors
202
most psychiatric disorders have a
significant genetic component and environmental factors
203
schizophrenia
positive symptoms, negative symptoms and cognitive dysfunction
204
bipolar disorder
cyclic mood disorder characterized by episodes of mania and depression
205
major depressive disorder
mood disorder characterized by depressive episodes
206
anxiety disorders
excessive anxiety
207
ADHD
primarily a disorder of the prefrontal cortex; executive function and maintaining attention
208
pathophysiology of ADHD
dysregulation of dopaminergic and adrenergic systems
209
Schizophrenia
characterized by positive symptoms, negative symptoms and cognitive impairment
210
example of a positive symptom
hallucination
211
example of a negative symptom
reduced motivation
212
the most disabling disorder
schizophrenia
213
dopaminergic hypothesis
inc in dopaminergic activity in mesolimbic, decrease in mesocortical, imbalance leads to schizophrenia
214
mood disorders
affect a person's emotional state
215
most common mood disorders
depression and bipolar disorder
216
Depression
at least one episode of depression (persistent sadness or loss of interest along with other symptoms)
217
monoamine hypothesis
normal amount of monoamine NT becomes reduced, depleted, or dysfunctional, depression occurs
218
HPA axis
hypothalamic pituitary axis; activated by stress
219
overreactive HPA
in states of chronic stress; associated with MDD and anxiety disorders
220
there is an association between elevated cortisol levels and
depression
221
spina bifida
most common NTD; one or more vertebrae fail to form a complete vertebral arch for enclosure of the spinal cord
222
Neuronal tube defects
stop in normal development of the brain and spinal cord during the first month of development
223
why is supplementation of folic acid important?
deficiency in B9 could increase risk for NTDs
224
when should folic acid supplementation begin?
before conception
225
spina bifida occulata
small gap in spine, no protrusion
226
meningocele
meninges protrude outward
227
myelomeningocele
spinal cord and meninges protrude outward leading to spinal cord damage
228
autism
bio-neurological developmental disability, appears before the age of 3
229
individuals with autism also suffer from
numerous comorbid medical conditions
