Neurological Disorders Flashcards

1
Q

Blunt Brain trauma

A

Closed
Head strikes hard surface or a rapid moving object strikes the head.
Dura mater is intact and brain tissue is not exposed.

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2
Q

What kind of brain injury can Blunt trauma cause?

A

Focal (local) or diffuse (general) brain injuries.

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3
Q

Open Brain Trauma

A

Penetrating

injury breaks the dura and exposes the cranial contents to the environment.

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4
Q

what kind of injury does open trauma cause?

A

Causes primarily focal injuries.

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5
Q

What are types of injury caused by Bunt Trauma?

A

Coup injury and Contrecoup

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6
Q

Coup Injury

A

Injury directly at the point of impact

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7
Q

Contrecoup

A

Injury on the polar opposite of the site of impact

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8
Q

Focal Brain Injury

A
Observable brain lesion 
force of impact typically produces contusion 
-extradural hematoma
-subdural hematoma
-Intracerebral hematomas
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9
Q

What are different types of concussions?

A

Mild and classical

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10
Q

Mild concussion

A

temporary axonal disturbance causing attention and memory deficits but NO loss of consciousness

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11
Q

Type I mild concussion

A

confusion
disorientation
memory amnesia

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12
Q

Type II Mild concussion

A

momentary confusion

retrograde amnesia of prior minutes

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13
Q

Type III Mild concussion

A

confusion with retrograde (greater than a few minutes) and anterograde amnesia

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14
Q

Classic concussion

A

Grade IV
loss of consciousness (for more than 6 hrs)
physiological and neurologic dysfunction without substantial anatomic disruption
anterograde and retrograde amnesia

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15
Q

What causes the loss of consciousness in grade IV concussions?

A

Disconnection of cerebral systems from the brain stem and reticular activating system

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16
Q

Your friend takes a huge hit as he is running for the goal line playing “flag football”. He is slow to get up and unsteady on his feet. He goes over to the sidelines and can’t remember what day of the week it is. The next day, he still can’t remember what happened for several hours before or after the game. How severe was the concussion he just experienced?

A

Grade III

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17
Q

cerebrovascular Disorders

A

Any Abnormalities of he brain caused by a pathologic process in the blood vessels

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18
Q

Cerebral Infarction

A

loss of blood flow to brain area

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19
Q

Cerebral Hemorrhage

A

Bleeding within the brain

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20
Q

Transient Ischemic Attacks (TIA)

A

confusion
difficulty communicating
usually no long term dysfunction (<24hrs)
a warning sign of something more severe.

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21
Q

What are different types of cerebrovascular accidents?

A

Hemorrhagic Stroke
Thrombotic Stroke
Embolic Stroke

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22
Q

Hemorrhagic Stroke

A

intracranial/cerebral hemorrhage
from an aneurysm
most common cause is hypertension

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23
Q

Thrombotic Stroke

A

arterial occlusions caused by thrombi formed in arteries supplying the brain or in the intracranial vessels

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24
Q

embolic stroke

A

an thrombus formed outside the brain

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25
Q

What are examples of Intracranial Aneurysms?

A

Saccular (berry) Aneurysms

Fusiform (giant) aneurysms

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26
Q

Saccular (berry) aneurysms

A

Exacerbated (caused) by hypertension
increases risk of hemorrhage
the walls move out on one side of the vein, kinda like it’s gonna go through exocytosis

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27
Q

Fusiform (giant) Aneurysms

A

walls move out on both sides like when you blow up ling skinny balloons

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28
Q

Cavernous Angiomas

A

group of dilated blood vessels with no other brain tissue

these are not that dangerous because they rarely hemorrhage.

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29
Q

capillary telangiectasis

A

small abnormally dilated capillaries. These are not that dangerous because they rarely hemorrhage.

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30
Q

venous angioma

A

abnormal cluster of veins draining a region of brain tissue. These are not that dangerous because they rarely hemorrhage.

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31
Q

Arteriovenous malformation (AVM)

A

most lethal
arteries and veins in tangle of malformed vessels
“tangle of worms”

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32
Q

Cerebral edema

A

increase in the fluid (intracellular or extracellular) with the brain

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33
Q

What are different types of cerebral edema?

A
vasogenic
cytotoxic
ischemic
interstitial 
Hyrdocephalus
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34
Q

Vasogenic edema

A

increased capillary permeability

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35
Q

cytotoxic edema

A

block active transport

problem transporting ions so you get water movement due to ion imbalances

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36
Q

ischemic Edema

A

follows cerebral infarction
increased capillary permeability
block active transport (ion imbalances)
water movement

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37
Q

interstitial edema

A

CSF moves across ependymal cells from ventricles to interstitial space

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38
Q

Hydrocephalus

A

type of interstitial cerebral edema

result of excess fluid within the cranial vault, subarachnoid space, or both.

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39
Q

What is hydrocephalus caused by?

A

an interference in CSF flow.

  • decreased reabsorption
  • increased fluid production
  • obstruction within the ventricular system
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40
Q

snout reflex

A

lips purse whenever touched lightly

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41
Q

palmomental reflex

A

twitch of cheek when stroking the palm

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42
Q

cerebral death

A

irreversible coma

death of the cerebral hemispheres exclusive of the brainstem and cerebellum

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43
Q

do you have behavioral or environmental responses in cerebral death?

A

No.

44
Q

which functions are normal during cerebral death?

A

respiratory, cardiovascular, temperature control, and GI function.

45
Q

survivors of cerebral death

A

remain in coma
emerge in a vegetative state
-akinetic mutism (AM)
-Locked-in syndrome

46
Q

Akinetic mutism

A

less aware

47
Q

locked-in syndrome

A

more aware

48
Q

seizures

A

disruption in balance of excitation and inhibition signals

49
Q

the sudden transient alteration of brain function in seizures is caused by:

A

an abrupt explosive disorderly discharge of cerebral neurons

50
Q

convulsion

A

tonic-clonic (jerky, contract-relax) movements associated with some seizures.

51
Q

generalized seizures

A

bilateral

52
Q

partial (focal) seizures

A

unilateral

53
Q

status epilepticus

A

experience of a second seizure before the person has fully regained consciousness/capacity from the preceding seizure or a singe seizure lasting more than 5 minutes

54
Q

what are some consequences of seizures

A

250% increase in adenosine triphosphate (ATP) demand
cerebral oxygen consumption increased by 60%
cerebral blood flow also increases aprox 250%
available glucose and oxygen are depleted

55
Q

what are some consequences of the depletion of available glucose and oxygen during seizures?

A

may produce secondary hypoxia and acidosis

may result in progressive brain tissue injury and destruction

56
Q

epilepsy

A

to be seized by a force from without

57
Q

two signals of seizure

A

aura

prodroma

58
Q

aura

A

partial seizure prior to “real” seizure

59
Q

prodroma

A

some sign like headache prior to seizure

60
Q

treatment for seizure syndromes

A

fat-rich diet reduces seizure frequency

61
Q

Cerebral edema caused by increased capillary permeability would be called:

A

Vasogenic

62
Q

multiple sclerosis

A

destruction of the CNS due to inflammation of the vessels in the CNS and demyelination of nerve cells. A development of scars throughout the CNS

63
Q

What is the cause of MS

A

interaction between autoimmune conditions, genetic make-up and viral infections of the brain.
(herpes simples and epstein barr)

64
Q

what are clinical manifestations of MS?

A

they are highly variable. It can attach any part of the CNS at any time. Which can cause problems with motor, sensory, cognitive, or autonomic system function.

65
Q

how do you diagnose MS?

A

High IgGin CSF

multiple lesions throughout the CNS detected by MRI.

66
Q

when does MS usually happen?

A

between 20-40 yrs old.

67
Q

in which gender is MS more prevalent?

A

females (2:1)

68
Q

where is MS more common?

A

the further away from the equator you are.

69
Q

what type of disease is MS thought to be

A

autoimmune

70
Q

What are the different types of MS

A

mixed (general)
spinal
cerebellar

71
Q

Mixed MS (general)

A

commonly have central problems (vision disturbances, memory deficits, mood alterations) along with motor/sensory impairments

72
Q

Spinal MS

A

mostly sensory and motor deficits

73
Q

Cerebellar MS

A

mainly motor-loss of coordination

74
Q

what are some treatments for MS?

A

prednisone (or other anti-inflammatory steroids) to decrease inflammation
interferon beta 1b and beta 1a
estrogen (clinical trials) for women

75
Q

Acute confusion states

A

mental disorder with deficits in attention and coherence of thoughts and action
-secondary to drug intoxication, metabolic disorder, or nervous system disease

76
Q

dementia

A

progressive failure of cerebral functions not caused by an impaired level of consciousness

77
Q

classifications of dementia

A

cortical

subcortical

78
Q

cortical dementia

A

alzheimers disease

79
Q

subcortical dementia

A

parkinson and huntington disease

80
Q

Alzheimers disease

A

most common neurodegenerative disease worldwide

81
Q

what causes alzheimer’s disease

A

degeneration of the brain manifested by:
-morphological changes
-biochemical changes
relates to genetic factors and poorly identified environmental factors.

82
Q

Morphological changes in Alzheimer’s disease

A

decreases surface area of the brain due to a decrease in size of the folds
neurofibrillary tangles
senile plaques
decreased blood flow to the brain

83
Q

neurofibrillary tangles

A

intracellular tangles of microtubules and microfilaments (detected upon autopsy)

84
Q

senile plaques

A

areas of degenerated cells that coalesce around a fibrous core (detected upon autopsy) formed from a protein named beta amyloid

85
Q

Clinical Manifestations of alzheimer’s disease

A

slow and progressive change in memory (recent memory loss first)
changes in mood
changes in motor function (late)

86
Q

Our results suggest that _________levels may be a risk factor for dementia, even among
persons without diabetes

A

higher glucose

87
Q

alzheimers disease is typifies by ______

A

amyloid plaques

88
Q

_____ enhances breakdown of amyloid

A

ApoE

which then prevents plaques

89
Q

how is insulin resistance related to alzheimer’s disease?

A

insulin resistance reduces cognitive function

90
Q

insulin resistance _____ risk of dementia

A

increases

91
Q

ketones _____ cognitive function

A

improve

92
Q

is there an approved test for early diagnosis of alzheimers disease?

A

No :(

93
Q

how do we diagnose alzheimers disease?

A

by ruling out other diseases and following the course of the disease

94
Q

what are some preventative measure for alzheimers’

A
diet rich in folate
reduce refined carbs
insulin-sensitizing meds
increase essential fatty acids
physical activity 
mental exercise
95
Q

what is treatment for alzheimers?

A

there is no cure

96
Q

Parkinson’s disease

A

destruction of brain dopamine neurons in the striatum and substantia nigra

97
Q

functional dopamine

A

coordinate the brain centers that monitor body position
involved in neuronal circuits that permit pre-programmed movements (movements w/o thinking)
inhibits the acetylcholine that cause muscle movement (reduces spontaneous, involuntary movements)

98
Q

Clinical manifestations of parkinson’s disease

A
tremor at rest 
rigidity 
akinesia (pill rolling)
dementia, slow thought process, or depression 
shuffling gait 
frozen face
postural abnormalities
disorders of righting and equilibrium
99
Q

Diagnosis for parkinsons

A

case history, course of disease, and brain scans

100
Q

environmental factors relates to parkinsons:

A
head trauma
exposure to anesthetics
exposure to hydrocarbons 
pesticide exposure
drinking well water 
working with wood or wood products
with in janitorial services
101
Q

Treatment of Parkinsons

A

Levodopa (Ldopa) precursor to DA.
dopamine agonists
inhibitor of monoamine oxidase (the enzyme taht degrades DA)
electrode placed in basal ganglia of the brain

102
Q

Huntington Disease is autosomal ____

A

dominant

103
Q

Huntington disease

A

a type of chorea (family of dyskinesias)
sever degeneration of the basal ganglia and frontal cerebral cortex
disrupted thought process

104
Q

clinical manifestations of huntington’s

A
abnormal movement (hyperkinesia)
dementia characterized by irritability (often becomes violent), apathy, inability to plan and organize, loss of short term memory, and slow thinking. 
euphoria or depression (bipolar, swing back and forth)
changes in different parts of the bain (basal ganglia) detected by MRI
105
Q

is there a treatment of huntington’s

A

no