Part 37 Flashcards

1
Q

90% of neurons in the body are what type? Where do they reside?

A

Interneurons/association neurons, between sensory and motor pathways in the CNS

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2
Q

Cerebellum acts as a ____ between movement ____ vs movement ____ to modify actions

A

Comparer, intended, actualized

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3
Q

Majority of all sensory information is….

A

….ignored (for example the constant noise in surroundings)

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4
Q

Spinal cord level circuits that do not require simple conduit of signals from periphery of body to brain and vise versa (4)

A
  • Walking circuits
  • withdrawal reflexes
  • support against gravity circuits
  • other reflex control of organ function such as defecation and micturition
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5
Q

2 divisions of afferent division of PNS

A

Visceral sensory division and somatic sensory division

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6
Q

2 divisions of efferent division of PNS

A

Viceral motor division to cardiac, smooth muscle, and glands (autonomic, sympathetic and parasympathetic) and somatic motor division to skeletal muscle

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7
Q

Electrical synapses definition and locations they are found (3)

A

Electrical current passing from cell to cell often thru gap junctions that is not common in the CNS or the body except in certain areas, useful to rapidly recruit and conduct more quickly than thru chemical synapses

  • retina
  • olfactory bulb
  • smooth and cardiac muscle
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8
Q

Chemical synapses

A

More common method of synapse in the body thru release of neurotransmitters (chemical messengers)

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9
Q

Neurotransmitters

A

One of over 40 compounds that are used in neuron communication thru release into the synapse that can then excite/inhibit postsynaptic neuron at a receptor, one way and thus allows signals directed toward a specific goal, must be present in nerve terminal, released during action potential, and have reproducible effect

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10
Q

2 structures important to function of synapse

A
  • presynaptic vesicles housing the neurotransmitter
  • mitochondria to provide energy to produce neurotransmitter
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11
Q

Axodendritic, axosomatic, and axoaxonic synapses

A
  • Where the axon of one neuron synapses on the dendrite of the other
  • Where the axon of one neuron synapses on the body of the other
  • Where the axon of one neuron synapses on the axon of another
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12
Q

Number of synapses on a postsynaptic cell is variable based on…

A

….decision making capacity of that postsynaptic cell (for example cerebellum receives many more than a spinal motor neuron)

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13
Q

Quantum

A

Several thousand molecules of neurotransmitter stored in synaptic vesicles at the nerve terminals kept relatively constant thru reabsorption or degradation to maintain a relative constant amount

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14
Q

Neuropeptides vs small molecule neurotransmitters

A

Neuropeptides are stored in larger granules that act at lower conc. and have longer lasting effects, with some functioning hormonally as well and being released from other tissue unlike small molecule neurotransmitters

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15
Q

Lock and key fit

A

Idea that only specific neurotransmitters or very closely related substances can bind to a specific receptor

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16
Q

What determines if a neurotransmitter is excitatory or inhibitory?

A

The receptor it binds (heart ones may be inhibitory while skeletal muscle are excitatory for the same neurotransmitter)

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17
Q

Neuromodulators and an example

A

Hormones, neuropeptides, or other messengers that modify synaptic transmission, act pre or postsynaptically to influence likelihood an AP will result in production of an AP in post synaptic terminal (ex - nitric oxide released by postsynaptic neurons diffuses into presynpatic neurons and stimulates release of more neurotransmitter)

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18
Q

Ca2+ mech of neurotransmitter release

A

Depolarization of presynpatic membrane by action potential opens voltage gated Ca2+ channels, influx of Ca2+ induces release of neurotransmitter thru unknown mechanism resulting in exocytosis via fusion of the vesicle to the membrane

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19
Q

Transmitters that open ____ excite postsynaptic neuron (depolarization), transmitters that are open ___ inhibit the postsynaptic neuron (hyperpolarization)

A

sodium channels, chloride channels

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20
Q

Secondary messenger activators

A

Cause prolonged changes in activity of neurons from seconds to months, some processes like memory require long term changes in neuronal activity in function, about 75% transduced via G protein coupled receptors, upon binding a portion of G protein dissociates and perform different functions

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21
Q

4 changes G protein bring about in post synaptic membrane

A
  • Opening specific ion channels in the post synaptic membrane
  • activation of an enzye system in cells membrane
  • activation of one or more intracellular enzymes
  • activate gene of transcription
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22
Q

Inactivation of ___ is acheived by phosphodiesterase

A

cAMP

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23
Q

Ways neurotransmitters are removed from synaptic cleft and ensure short term effect on post synpatic terminals

A
  • Catabolism of enzymes located near receptor
  • active transport(quickly pump back in nerve terminals)
  • diffusion (into extracellular fluid
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24
Q

More ___ a neuron has the greater its info processing capability

A

-Synapses

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25
Q

Excitatory postsynaptic potential (EPSP) and 2 examples

A

A positive voltage change causing postsynaptic cell to become more likely to fire (depolarization) resulting from Na+ flowing into cell,
-glutamate and aspartate

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26
Q

Inhibitory postsynaptic potential (IPSP) and 2 examples

A

A neg voltage change causing postsynaptic cell to be less likely to fire (hyperpolarization) resulting from Cl- flowing into cell or K+ leaving the cell
-glycine and GABA

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27
Q

What 2 neurotransmitters can be either EPSP or IPSPs?

A

Ach and norepi

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28
Q

Normal resting membrane potential and general distribution of Na, K, Cl, and protein anions

A

-65mV due to excess Na+ outside, K+ inside, Cl- outside, and proteins and such inside (neg charged)

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29
Q

Nernst potential

A

Potential that exactly electrically opposes the movement of an ion across the neuronal membrane down its conc. gradient (electrochemical equilibrium of a particular ion), determined by the balance when conc. gradient and electric gradient directly oppose each other (61mV for Na+ to prevent influx, -87mV for K+ to prevent efflux, and -69mV in Cl- to prevent influx)

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30
Q

Threshold value for neuronal AP

A

Potential required for opening of voltage gated sodium channels causing rapid movement of Na+ inward in a neuron

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31
Q

Excitatory cholinergic synapse mech of action

A
  • Ach crosses synapse
  • Ach receptors trigger opening of Na+ channels producing local potential
  • Upon reaching -55 mV see AP triggered
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32
Q

Inhibitory post synaptic potential mech of action

A

-Inhibitory synapses open K+ or Cl- channels causing hyperpolarization of neuron, cell membrane potential becoems more negative resulting in inhibitory post synaptic potential (-65 to -90mV)

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33
Q

Presynaptic inhibition, what neurotransmitter does this?

A
  • Activation of presynaptic synapses decreasing ability of Ca2+ channels to open on the presynaptic terminals resulting in reduced neurotransmitter release
  • Typically facilitated by GABA
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34
Q

When action potentials from peripheral baroreceptors begin firing very frequently due to high pressure, this is relayed to the brain to cause what physiologic response?

A

Vasodilation

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35
Q

Criteria for a chemical to be considered a neurotransmitter (3)

A
  • chemical must be present in nerve terminal
  • chemical must be released from nerve terminal by action potential
  • chemical when applied experimentally to receptor must produce identical effect
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36
Q

Example of a small molecule neurotransmitter and example of a neuropeptide

A
  • GABA
  • cholecystokinin or B endorphins
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37
Q

2 components of receptors on postsynaptic membranes

A
  • Binding component
  • Ionophore component (opens an ion channel or activates 2ndary messenger system
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38
Q

75% of second messenger activators are ____. How do these systems work?

A

G protein coupled receptors, work thru dissociation with alpha portion moving about cytoplasm and either oopening an ion channel, activating an enzyme system, or allowing gene transcription

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39
Q

Ability to process, store, and recall info is due to…

A

….neural integration

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40
Q

Neural integration is based on…

A

….types of postsynaptic potentials produced by neurotransmitters (excitatory or inhibitory)

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41
Q

Excitatory adrenergic synapse mech of action

A
  • NE binds receptor on post synaptic cell
  • activates cAMP
  • wide variety of effects such as activating enzymes and opening ligand gates
  • post synaptic potential formed
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42
Q

GABA is ____ through producing ___polarization

A

inhibitory, hyper

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43
Q

Facilitation of neurons

A

When a neuron potential is closer to threshold than normal but not yet to firing level that can be easily stimulated by summated by subsequent input

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44
Q

2 types of summation of postsynaptic potentials

A

Spatial - multiple terminal excitation simultaneously by an EPSP exceeding threshold for inducing action potential
Temporal summation - when post synaptic neuron is stimulated repeatedly by the same presynaptic neuron, with more rapid firing of EPSP in shortened period of time can exceed threshold for inducing action potential

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45
Q

Macro example of summation in action

A
  • Accidentally touching a hot pan on stove results in EPSPs in motor neurons causing hand to jerk back quickly
  • Intentionally touching a hot pot of coffee keeps you from withdrawing and dropping it by having IPSP’s dominating effect overriding the EPSPs
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46
Q

Synaptic fatigue

A

Occurs when exhaustion of stores of transmitter in synaptic terminals occurs

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47
Q

Post tetanic facilitation

A

Enhanced responsiveness following repetitive stimulation due to build up of Ca2+ ions in presynaptic terminals causing more vesicular release of transmitter

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48
Q

Synaptic delay

A

Depending on length of delay of neurotransmission, can calculate number of neurons in a circuit

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49
Q

Effect of acidosis, alkalosis, and hypoxia on neuronal activity

A
  • depresses
  • increases excitability (seizures)
  • can’t go long without!
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50
Q

Neural coding of qualitative vs quantitative info

A
  • Qualitative depends on which neurons are fired
  • quantitative depends on # of neurons recruited with stronger stimuli causing more rapid firing rate
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51
Q

Threshold, maximal, submaximal, supramaximal stimuli

A

Threshold causes AP, maximal is max # of AP that can be generated per unit time, submaximal is between threshold and maximal, supramaximal sees no more frequency than max in # of AP that can be generated

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52
Q

Parkinsonism vs parkinson disease (what is a defining characteristic that makes parkinson’s disease stand out)

A

Parkinsonism is the clinical syndrome presenting with any combo of bradykinesia, rest tremor, rigidity, and postural instability with the most common cause being parkinson’s disease but there are many others, vs parkinson’s disease is a chronic progressive disorder caused by degenerative loss of dopaminergic neurons in the brain characterized clinically by aysmmetric parkinsonism (defining trait) and a clear dramatic benefit from dopaminergic therapy

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53
Q

TRAP acronym for parkinsonism

A

rest Tremor
Rigidity
brady or Akinesia
Postural instability

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54
Q

Differential diagnosis of parkinsonism (4)

A
  • Parkinson disease (most common)
  • Dementia with lewy bodies
  • Multiple system atrophy
  • Huntington disease
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55
Q

Dementia with Lewy bodies

A

-Second most common form of degenerative dementia characterized by early psychotic symptoms (unlike parkinsons which that is late stage), see fluctuations in attention or level of arousal and protein aggregate buildups called lewy bodies in neurons and REM sleep disorder behavior disorder (act out dreams)

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56
Q

Multiple system atrophy (what is its one unique characteristic)

A

A slightly more common parkinsonism disease in men than women that causes autonomic dysfunction, cerebellar signs, and parkinsonism that is poorly responsive to levodopa therapy with a median survival rate of 6-9 years but is always bilateral (not asymmetric), lacks rest tremor or cortical sensory loss.
-Characteristic finding is stimulus sensitive myoclonic jerk

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57
Q

3 subtypes of multiple system atrophy

A

Shy drager syndrome, striatonigral degeneration, olivapontocerebellar atrophy

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58
Q

Multiple system atrophy treatment (1)

A

-palliative symptomatic treatment

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59
Q

Progressive supranuclear palsy

A

A rare form of parkinsonism characterized by early instability with falls, failure to respond to levodopa therapy, and marked slowing of vertical gaze (especially downward) with a median survival rate of 5-9 years but is always bilateral, lacks rest tremor or cortical sensory loss

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60
Q

Corticol basal degeneration

A

Form of parkinsonism with insidious onset and progression of ASYMMETRIC cortical and basal ganglionic features, speech impairment, cortical dysfunction, and abnormal slow horizontal saccades (slow moving compared to nystagmus)

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61
Q

Essential tremor

A

Most common neurologic of an action tremor that usually affects hands and arms but also head, chin, trunk, and legs. Not commonly isolated tremor, and often becomes readily apparent when arms arms outstretched or engaged in activities such as writing

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62
Q

Depression and Parkinsonism

A

Often may see overlap in symptoms such as flat affect, bradykinesia, decreased appetite making it hard to differentiate source

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63
Q

Idiopathic and familial basal ganglia calcification/fahr disease

A

A type of parkinsonism that is due to accumulation of calcium in the basal ganglia (but not other parts of body) that then results in early age onset (as early as 20) parkinsonism

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64
Q

Common causes of secondary parkinsonism (7)

A
  • Antipsychotropic agents (can take a while to develop effects, remit after cessation)
  • toxins (cyanide poisoning can mimick)
  • head trauma
  • lesions
  • metabolic disorders
  • infection (toxoplasmosis in cat poop)
  • CVD
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65
Q

Pseudohypoparathyroidism

A

A secondary cause of parkinsonism from high parathyroid hormones but low blood Ca2+ due to resistance in response of the body in the pathway to increase levels

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66
Q

Vascular parkinsonism

A

A type of parkinsonism caused by its primary risk factor CVD, do NOT see rest tremor but do see prominent instability and gait disorder

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67
Q

Normal pressure hydrocephalus

A

Syndrome of urinary incontinence, gait dysfunction, urinary incontinence, and cognitive impairment that may mimic symptoms of parkinsonism but can be differentiated by seeing ventricular enlargement on CT/MRI and improvement upon shunting treatment

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68
Q

rabbit syndrome

A

Type of drug induced parkinsonism that is an adverse effect of antipsychotic meds for which perioral tremors that spare the tongue occur that resemble a rabbit’s nose

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69
Q

Huntington’s disease

A

Genetic anomaly that causes chorea type movements in early stage but can mimic parkinsons in end stage

70
Q

Restless leg syndrome

A

Occurs in up to 15% of population, sleep related disorder causing unpleasant or uncomfortable urge to move legs that is relieved upon motion, makes it hard to sleep and can cause periodic movement during sleep, suspected to be related to low iron stores and is dopamine related to some degree, treatment with dopamine agonist but try to avoid benzos or opioids

71
Q

Malignant neuroleptic syndrome definition, clinical symptoms, and treatment

A
  • Life threatening neurologic emergency associated with use of antipsychotic agents that leads to systemic complications
  • clinical symptoms see rigidity, fever, mental status changes, and believed to be from dopamine receptor blockade.
  • Treated thru cessation of offending agent
72
Q

Domperidone

A

Non approved US medication that is an antiemetic that requires closely monitoring to prevent progression to neuroleptic malignant syndrome but is used to treat gastroparesis

73
Q

Distinguishing features of parkinsonism from parkinson disease (5)

A
  • Falls at presentation and early disease course unlikely to be PD
  • poor response to levodopa
  • symmetry of onset
  • rapid progression
  • lack of tremor
74
Q

Parkinson disease epidemiology

A

1% of population by age 65, 5% by age 85, most common neurodegenerative movement disorder

75
Q

Parkinson disease pathophysiology

A
  • Brought on by degeneration of dopaminergic neurons in the substantia nigra par compacta of the midbrain resulting in intracytoplasmic inclusions known as lewy bodies and deposition of a-synuclein that then spreads out to rest of brain in chronic progressive disease, asymptomatic until 60% of neurons have been lost
  • precise mech not understood but likely a complex interaction of genetic abnormalities and oxidative stress, etc.
76
Q

Substantia nigra

A

Part of brainstem midbrain that is a dark streak composed of pars compacta and pars reticulata, with pars compacta having a dense conc. of dopamine neurons and pars reticulata having GABA neurons. These motor pathways play a significant role in motor function and thus is significantly damaged in disease states like parkinsons

77
Q

Clinical presentation of parkinson’s disesase (9)

A
  • Resting tremor 3-7 Hz
  • pill rolling motion
  • tremor stops upon intention and returns upon distraction
  • tremor unilateral initially then becomes bilateral
  • distal to proximal bradykinesia
  • cogwheel rigidity on the same side as the tremor
  • micrographia
  • shuffling gait that gets progressivley faster
  • anosmia in early early onset***
78
Q

Diagnosis of parkinson’s disease (1)

A

Clinical diagnosis, MRI and dopamine tag scanning are useful for ruling out but none are diagnostic

79
Q

Parkinson disease treatment options

A

-PT/OT/speech therapy

-

80
Q

Delayed therapy of parkinson’s treatment

A

Debate if it is worth to start early med because no evidence if it improves any outcome and has bad side effects so must weigh better or worse

81
Q

Therapeutic options for Parkinson’s disease (4)

A
  • Levodopa/carbidopa (replaces dopa in brain, on off fluctuations are complications and bad other side effects, gold standard most effective/carbidopa prevents conversion of dopa to dopamine in periphery)
  • anticholinergics (assist with tremor)
  • MAOB inhibitors (delays breakdown of dopamine allowing it to be in receptors longer)
  • Catechol o methyl transferase inhibitors (prevents transferase from degrading neurotransmitters)
82
Q

Cerebrovascular disease

A

A collective term for a range of conditions that affect and decrease blood flow to brain such as carotid stenosis, aneurysms, vascular malformations, stroke, etc.

83
Q

Risk factors for CVD (also which is MOST important?) (8)

A
  • HTN (MOST important)
  • atherosclerosis
  • hyperlipidemia
  • diabetes
  • smoking
  • diet
  • obesity
  • increasing age/male/african americans
84
Q

Carotid stenosis definition, when is it symptomatic, diagnostic studies (3), treatment options

A
  • A type of cerebral vascular disease caused by atherosclerosis plaque in the arteries that are main supply to brain
  • Often asymptomatic until a TIA
  • PE might find carotid bruit, doppler ultrasound, or cerebral angiography
  • In less than 50% occlusion treated conservatively with antihypertensives, statins, anticoags while >50% require stenting but NOT endarterectomy (too risky)
85
Q

Cerebral aneurysm causes (4), epidemiology, types, signs/symptoms, diagnosis

A
  • Caused by hypertension, atherosclerosis, trauma, congenital defect
  • most prevalent in ages 50-60 and more common in women
  • 2 types: saccular (rounded outpouching containing blood also called berry) and fusiform (balloons or bulges out on all sides of artery)
  • Signs and symptoms unruptured are asymptomatic but occasionally have cranial nerve palsy, dilated pupils, double vision, or pain - ruptured have localized headache, nausea and vomiting, stiff neck
  • Diagnosed via MRA and carotid angiogram, rupture can also be detected by CT or lumbar puncture then cerebral angiography
86
Q

Vertebrobasilar insufficiency cause, signs/symptoms, diagnosis (2), treatment options (3)

A
  • Caused by decreased blood flow to vertebral and basilar arteries, affects the brainstem, occipital lobes, and cerebellum
  • vision loss, diplopia, vertigo, dysarthria, ataxia, confusion
  • MRA or angiography
  • lifestyle modifications, meds, surgery
87
Q

Arteriovenous malformations definition, cause, signs/symptoms (2), diagnosis (2), treatment (1)

A
  • Groups of abnormal/poorly formed blood vessels resulting in increased rate of bleeding
  • typically congenital found incidentally
  • seizure and headache (4/100 people will hemorrhage per year)
  • MRI and angiography
  • Treated by neurosurgery
88
Q

Stroke definition, how does it clinically present?

A
  • Abrupt onset of neurological deficit attributable to focal vascular disease, acute brain injury caused by decreased blood supply (ischemia) or hemorrhage
  • clinical manifestations are variable because of the complex anatomy of the brain and its vasculature
89
Q

Stroke is a ____ diagnosis

90
Q

Stroke pathophysiology

A
  • Brain is 2% of body weight but takes 17% of cardiac output and 20% o2
  • ischemia is caused by decrease in blood flow that lasts longer than a few seconds
  • neurons lack glycogen so energy failure is rapid and necrosis occurs faster than in other tissue
91
Q

Stroke epidemiology

Stroke is the leading cause of what?

A
  • 5th leading cause of death, 87% are ischemic rather than hemorrhagic,
  • leading cause of serious long term disability
92
Q

2 types of stroke based on dysfunction and their subclasses

A
  • focal brain dysfunction (ischemic and intracerebral hemorrhage)
  • diffusion brain dysfunction (subarachnoid hemorrhage)
93
Q

80% of ischemic strokes occur from occlusion of ____ caused by _____.

Majority of strokes are ____ rather than ____

A
  • large or small vessels
  • thrombosis (clot), embolism (dislodged flowing object), or systemic hypoperfusion (circulatory problem of whole brain)
  • ischemic, hemorrhagic
94
Q

Ischemic stroke vs TIA

A

Ischemic stroke is infarction with sequelae (symptoms don’t completely go away while body tries to compensate) vs TIA has no infarction and no sequelae but is a transient “mini stroke”

95
Q

Transient ischemic attack (TIA)

A

Transient episode of focal ischemic cerebral neurologic deficits without infarction, symptoms typically less than 1 hour but varies, risk of stroke rises if not treated early enough

96
Q

Transient ischemic attack clinical presentation (3) and which set of symptoms does carotid TIA belong to and which does vertibrobasilar ischemic belong to?

A
  • abrupt and rapid recovery
  • weakness and heaviness of contralateral arm, leg, or face with possible numbness (carotid)
  • vertigo, ataxia, diplopia, dysarthria, changes in vision (vertebrobasilar ischemic)
97
Q

TIA diagnostic studies (5)

A
  • CT of head
  • echo
  • EKG (afib)
  • CBC (infection)
  • blood glucose (hypoglycemia)
98
Q

TIA treatment options (4)

A
  • carotid endarterectomy if surgery accessible stenosis
  • anticoagulants
  • aspirin 325mg po daily
  • clopidogrel (plavix)
99
Q

Penumbra

A

Zone of reversible ischemia around core of irreversible infarct, salvageable in first few hours after ischemic stroke onset and goal to save with treatment to reverse and minimize permanent damage

100
Q

Lacunar infarct ischemic stroke definition and presentation (3)

A
  • A common type of ischemic stroke usually caused by small lesions often in patients with no memory of CVA found incidentally, usually progress over 24 hours then stabilize
  • Present with contralateral motor and sensory deficits, ipsalateral ataxia, and dysarthria
101
Q

Carotid circulation ischemic stroke definition and presentation (1)

A

-A common type of ischemic stroke that is usually asymptomatic but can present with amaurosis fugax (collateral circulation brings vision back)

102
Q

LEFT sided MCA ischemic stroke should raise worry for….

A

….broca’s or wernicke’s aphasia

103
Q

anterior cerebral artery ischemic stroke key points (2)

A
  • emotional symptoms
  • unilateral occlusion well tolerated because of collateral blood flow
104
Q

middle cerebral artery ischemic stroke key point (1)

A

-wernicke and broca’s aphasia if on left side of brain

105
Q

posterior cerebral artery ischemic stroke key points (2)

A
  • thalamic syndrome: contralateral hemisensory disturbance followed by spontaneous pain and increased sensation
  • memory loss
106
Q

Older infarcts often appear ____ while fresh appear ____ on a CT

A

Darker, lighter

107
Q

Anterior portion of pons locked in syndrome

A

An absence of movement except for eyelids despite sensation and consciousness preservation associated with incomplete occlusion of the vertebral or basilar arteries

108
Q

Patients having a stroke are generally not in….

A

….pain, they don’t seek assistance on their own (time is tissue)

109
Q

ED stroke care timeline

A

-Triage (10 min)
-medical care (25 min)
-CT and labs (45 min)
Treatment (60 min)

110
Q

NIH stroke scale (NIHSS)

A

Standardized method used to measure the level of impairment caused by a stroke, scored from 0-42 to determine the severity, includes CN, motor, sensory, cerebellar, inattention, language, etc.

111
Q

Differential diagnosis of stroke (5)

A
  • seizure
  • syncope
  • migraine
  • hypo/hyperglycemia
  • drug toxicity
112
Q

Stroke diagnostic studies (which is the most important) (6)

A
  • CT without contrast (most important)
  • Standard MRI
  • MRA
  • Angiography
  • EKG
  • CXR
113
Q

Labs to order in a suspected stroke patient (7)

A
  • Blood glucose
  • Troponin I
  • Pt/PTT
  • CBC with diff
  • Chem 7
  • lipid panel
  • urinalysis (looking for elicit drugs)
114
Q

Contraindications to treating ischemic stroke with tPA (3)

A
  • Recent surgery
  • GI bleed
  • High blood pressure even after treatment
115
Q

Ischemic stroke treatment options (2)

A
  • IV tPA
  • mechanical thrombectomy
116
Q

Many ischemic strokes present with ___ blood pressure. This is because….

A

high,
….it is a response, not a cause (don’t lower it unless its super high! (>185/110))

117
Q

Ischemic stroke supportive therapy (5)

A
  • fluids
  • glucose management
  • swallowing eval to prevent aspiration
  • treat fevers
  • seizure prophylaxis
118
Q

If a patient comes in with a stroke that is not a stroke center, best course of action is to…

A

….stabilize best as possible (prob give tPA) and then transfer to a stroke center

119
Q

CT/MRI appearance cannot determine the etiology of ____

A

Small cerebral infarcts

120
Q

Prescriptions post ischemic stroke as secondary prevention (4)

A
  • antithrombotic agent based on cause
  • ACEI or ARB regardless of BP
  • Statin regardless of cholesterol
  • lower BMI, alcohol intake, cigarrete smoking, estrogen
121
Q

Intracerebral hemorrhage definition

A

A type of hemorrhagic stroke from bleeding into the brain that spreads along white matter, occurs over minutes to hours and is progressive with gradual onset, not abrupt

122
Q

Subarachnoid hemorrhage definition

A

Type of hemorrhagic stroke that is most often caused by aneurysm rupture with bleeding into CSF, abrupt and severe thunderclap “worst headache of life” with no focal neuro symptoms but generalized vomiting and progressive impairment alongside nuchal rigidity

123
Q

One of the reasons important to get immediate CT in evaluation of stroke is to determine if patient has….

A

….hemorrhage which would contraindicate tPA and indicate immediate need for neurosurgery

124
Q

Biggest risk factor for intracerebral hemorrhage and 2 other ones(3)

A
  • Hypertension
  • aneurysm
  • cocaine or amphetamine use
125
Q

Lumbar puncture is contraindicated in a ___ hemorrhage but useful in a ____ hemorrhage

A

intracerebral, subarachnoid

126
Q

If CT is ___ on a subarachnoid hemorrhagic patient, then must perform ___ looking for ____

A

negative, lumbar puncture, xanthrochromia (yellowish appearance of CSF after bleeding)

127
Q

TIA’s should be treated as though they are….

A

….strokes

128
Q

Ischemic strokes of the vertebral or basilar arteries characteristics (4)

A
  • consciousness changes
  • vision deficits
  • coordination issues
  • lack of balance
129
Q

Ischemic strokes of the cerebellar arteries characteristics (3)

A
  • vertigo
  • nystagmus
  • ataxia
130
Q

Ischemic strokes of anterior spinal artery characteristics (2)

A
  • Flaccid paralysis below level of lesion
  • loss of sensation below level of lesion
131
Q

Ischemic strokes of posterior spinal artery characteristics (1)

A

-sensory loss

132
Q

In the initial assessment of the suspected stroke patient, provider should establish a…

A

….time of symptom onset (last known normal) as this will dictate the treatment

133
Q

MRI vs MRA

A

MRA is used specifically to examine blood vessels

134
Q

There are more consequences for doing what regarding tPA?

A

Not giving, compared to giving in case of acute treatment for ischemic stroke

135
Q

Intracerebral hemorrhage treatment options (3)

A
  • supportive care
  • intracranial pressure monitoring
  • potential neurosurgical consult
136
Q

Subarachnoid hemorrhage treatment options (4)

A
  • operative treatment
  • pain medication
  • gradual BP treatment but maintenance of DBP >100
  • prophylactic anti seizure medication such as pheyntoin
137
Q

Vertigo definition

A

Abnormal perception of movement typically described as spinning, floating, or ground rising or falling, associated with nausea and vomiting in severe cases

138
Q

Vertigo is a ___, not a ___

A

symptom, diagnosis

139
Q

Vertigo can be derived from a problem along these different areas (4)

A
  • Vestibular system
  • vestibulocochlear nerve (CN8)
  • semicircular canals
  • central vestibular structures in brainstem or cerebellum (TIA’s, tumors, MS)
140
Q

Vertigo epidemiology

A

Most commonly benign paroxysmal positional vertigo and vestibular neuritis (both benign), treated typically outpatient

141
Q

It is important to differentiate pure vertigo from these 2 conditions

A
  • unsteadiness/imbalance (parkinson’s)
  • lightheadedness/syncope
142
Q

Benign causes of vertigo arise in the ___, more urgent arise closer to the ___

A

periphery, CNS

143
Q

Common drugs that can result in drug induced vertigo (4)

A
  • Lasix
  • erythromycin
  • NSAIDS long term
  • tetracycline
144
Q

Nystagmus

A

Constant involuntary cyclic eye movements that can be caused by central or peripheral lesions either rotary, horizontal, or vertical

145
Q

Pure ___ or ___ nystagmus suggests a central lesion

A

vertical, torsional

146
Q

Nystagmus from peripheral cause tends to be…. (5)

A
  • unidirectional
  • horizontal with torsional component never purely torsional or vertical
  • suppressed with fixation
  • lack of ataxia, aphasia, hemiparesis
  • walking preserved
  • deafness or tinnitus may be present
147
Q

Nystagmus from central cause tends to be… (6)

A
  • Tends to be torsional or vertical
  • can change direction
  • not suppressed by fixation
  • often have ataxia, aphasia, hemiparesis
  • walking not preserved
  • no deafness or tinnitus
148
Q

Vestibular neuritis

A

Inflammation of the vestibulocochlear nerve presenting often subacute with nausea, vomiting, and gait instability (but hearing is intact) that resolves over days but can persist for months, usually viral and self limiting in healthy young people

149
Q

Labrynthitis

A

Vestibular neuritis combined with unilateral hearing loss

150
Q

Head thrust test and positive/negative interpretation

A
  • Patient fixates on target on wall while examiner moves head rapidly to each side looking for any movement of the pupil that if it moves sign of decreased neural input from ispalateral ear to vestibulocochlear reflex
  • Positive in vestibular neuritis, negative for CNS cause
151
Q

Vestibular neuritis treatment options (3)

A
  • Antiemetics
  • Steroids
  • vestibular rehab
152
Q

Benign paroxysmal positional vertigo (BPPV)

A

Leading cause of vertigo caused by calcium debris in the posterior semicircular canal causing a brief reproducible spinning sensation when turning or tilting head backwards asking only a couple seconds

153
Q

Dix-Hallpike maneuver and interpretation

A
  • Turn patients head to left and bring to supine position on table with head 20 degrees elevated above table for 30 seconds, then lifted and repeated on other side
  • positive indicates ipsalateral BPPV
154
Q

Epley maneuver

A

Physical manipulation from the dix hallpike maneuver to rotate prone in order to dislodge calcium deposits causing BPPV

155
Q

Herpes zoster oticus/ramsay hunt syndrome

A

Herpes zoster infection of part of facial nerve causing acute vertigo, hearing loss, ipsalateral facial paralysis, ear pain, and vesicles in the auditory canal

156
Q

Herpes zoster oticus/ramsay hunt syndrome treatment options (2)

A
  • Corticosteroids
  • acyclovir
157
Q

Meniere’s disease

A

Excess endolymphatic fluid pressure brought on by unknown cause resulting in recurrent attacks of vertigo usually unilateral associated with auditory symptoms (hearing loss, tinnitus, fullness in the ear), with nystagmus during attacks and gait imbalance/nausea/vomiting

158
Q

Meniere’s disease treatment (4)

A
  • Low salt diet
  • diuretics
  • avoid caffeine, chocolate, red wine
  • intratympanic gentamycin injections (permanent hearing loss)
159
Q

Perilymphatic fistulas, diagnosis (1), treatment (1)

A
  • Fistula at the oval or round window between inner ear and middle ear from head trauma, barotrauma, or heavy lifting causing episodic vertigo with hearing loss with coughing/sneezing
  • CT scan
  • Bed rest, avoid straining, resolves on own
160
Q

Labyrinthine concussion

A

Traumatic peripheral vestibular injury following direct concussive head trauma, more severe with temporal bone fracture can be permanent, while typically resolves in days to months

161
Q

Cogan syndrome and treatment (1)

A
  • Rare autoimmune condition causing interstitial keratitis (dry red eyes) and vestibuloauditory dysfunction (vertigo, tinnitus, hearing loss) that comes and goes
  • Systemic steroids
162
Q

Familial bilateral vestibulopathy

A

Brief attacks of vertigo (seconds in duration) followed by progressive loss of peripheral vestibular function leading to imbalance

163
Q

Vestibular schwannoma

A

Benign tumor of the 8th cranial nerve that can be seen on MRI that is a rare peripheral cause of vertigo

164
Q

Vestibular migraines

A

Migraines that present with vertigo and often mimic meniere’s disease but respond to medications for migraines

165
Q

Brainstem/cerebellar ischemia/infarction vertigo and 3 abnormal ocular motor findings

A
  • Caused by embolic or atherosclerotic occlusion of vertebrobasilar arterial system
  • spontaneous nystagmus purely vertical/horizontal/torsional, ataxia toward size of lesion, other neurological findings
166
Q

Wallenberg CVA

A

Specific type of brainstem infarct/dissection of the posterior inferior cerebellar artery causing infarction of the lateral medulla causing vertigo, nystagmus, and ataxia but also ipsalateral horner syndrome

167
Q

Horner syndome and its triad of presentation

A

Interruption of sympathetic nerve supply to eye characterized by

1) miosis
2) partial ptosis
3) anhidrosis (loss of hemifacial sweating

168
Q

___ type vertigo is made worse by head movement

169
Q

Following a CVA, reflexes are ___ immediately but few days after become ____

A

hyporeflexive, hyperreflexive

170
Q

Treatment for vertigo options (3)

A
  • Antivert (meclizine) 25-50mg TID
  • Corticosteroids
  • Phenothiazine antiemetics