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Neuroscience > Test 2 > Flashcards

Test 2 Flashcards

1
Q

What is the primary function of the ANS?

A 
Regulates homeostasis (maintenance of an optimal internal environment)
- circulation, respiration, digestion, metabolism, secretions, body temp, and reproduction
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2
Q

Thee divisions of the ANS:

A

1 Sympathetic
2 Parasympathetic
3 Enteric nervous system

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3
Q

Reticular formation

A

receives input from visceral receptors, the hypothalamus and the limbic system

  • the reticular formation then generates the appropriate responses for the ANS
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4
Q

Preganglionic neuron

A

neuron extending from the SC or brainstem

  • sympathetic - release ACh
  • parasympathetic release - ACH

Symp- arise in interomediolateral cell column T1-L3
Para- arise from CN(3,7,9,10) and S2-S4 spinal levels
**Symp are relatively SHORT
**Parasymp are relatively LONG

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5
Q

postganglionic neuron

A

neuron connecting with the target oran/ tissue
- sympathetic - release norepinephrine
parasympathetic- release ACh

  • *Symo are relatively LONG
  • **Parasymp are relatively SHORT
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6
Q

Sympathetic divisions responses

A 
"Fight of Flight"
pupil dilation
bronchodilation
cardiac acceleration
inhibition of digestion
piloerection
stimulation of glucose  release
systemic vasoconstriction

**energy expenditure

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7
Q

Parasympathetic division responses

A 
"Rest or Digest"
pupil constriction 
bronchoconstriction 
cardiac deceleration
stimulation of digestion
salivation, lacrimation
intestinal vasodilation

**Energy consevation

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8
Q

Sympathetic Neurons can synapse:

A
  1. immediately in the trunk
  2. after traveling up or down the trunk
  3. after passing through the trunk (in the periphery)
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9
Q

tentorial notch

A

opening in tentorium cerebelli

midbrain passes through the tentorial notch

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10
Q

epidural space

A

between inner skull and dura (potential space)

middle meningeal artery

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11
Q

middle meningeal artery

A

blood supply to dura
branch of external carotid artery
-commonly can hemmorrage leading to epidural hematoma

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12
Q

subdural space

A

between dura and arachnoid (potential space)

bridging veins cross over the subduralspace to drain into the dural venous sinuses

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13
Q

venous sinuses

A

large channels formed between the two layers of dura

  • drain venous blood and CSF into sigmoid sinuses to reach the internal jugular veins
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14
Q

subarachnoid space

A

between arachnoid and pia (actual space)

  • CSF filled
  • contains major arteries of the brain
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15
Q

arachnoid trabeculea

A

fine filaments loosely connecting arachnoid to pia

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16
Q

Perimesencephalic cistern

A

interpeduncular

quadrigeminal- superior and inferior colliculi

prepontine

cisterna magna
lumbar - functional importance for spine tap

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17
Q

blood brain barrier

A

in the brain capillary endothelial cells are joined at their edges
-most fat soluble and smaller molecules can clear wall

-BBB monitors and restricts entry of water soluble and large molecules (require active transport)

most drugs, viruses, radioactive ions and antibiotics cannot pass barrier

  • a blood-CSF barrier also exists between the choroid plexus and CSF
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18
Q

circumventricular organs

A

specialized brain regions where ther is no BBB
allows the blood to be monitored so the brain can respons to changes in the chemical environment of the rest of the body

EX: median eminence and neurohypophysis- regulation and release of pituitary hormones

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19
Q

Intracranial pressure

A

elevated ICP can cause decreased cerebral perfusion and brain ischemia
- normal ICP ~ 15mmHg
cerebral perfusion > 50mmHg

Large increases in ICP can happen suddenly or more slowly, leading to irreversible brain damage and death, sometimes within hours

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20
Q

common S/S of elevated ICP

A 
headache
altered mental status 
nausea
and vomiting
papilledema, visual  loss --> CN II
diplopia(double vision) CN VI
cushing's triad: HTN, bradycardia, and irregular respirations
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21
Q

Brain herniation syndromes

A

1 Subfalcine- cingulate gyrus under falx cerebri compress ACA

  1. ventral- Central and downward displacement of brainstem. CN VI can lead to uncal herniation
  2. Uncal herniation- Medial temporal lobe through tentorial notch. CN III (dilated pupil) contralateral hemiplegia, coma
  3. tonsillar- cerebellar tonsils through foramen magnum, Respiratory arrest, BP instability, death
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22
Q

epidural hematoma

A

potential sace between the dura and skull

  • usually from rupture of middle meningeal artery due to temporal bone fx
  • initially pt may have no sx’s but within a few hours leads to elevated ICP and herniation and death with no surgical TX

CT: lens-shaped hematoma

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23
Q

subdural hematoma

A

potential space between dura and arachnoid

  • rupture of bridging veins which are susceptible to shear injury as they cross arachnoiod into dura
  • venous blood spreads out over a large area and forms crescent shaped hematoma

2 types: Chronic, acute

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24
Q

Chronic subdural hematoma

A

commonin elderly patients
- brain moves more freely due to atrophy and bridging veins are more susceptible to shear injury
- can be from minimal trauma
0 venous blood slowly collects over a priod of weeks to months leading to vague sx’s

CT: chronic blood- hypodense

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25
Q

acute subdural hematoma

A

impact velocity must be quite high for significant subdural hematoma to occur right after an injury

CT: acute blood- hyperdense

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26
Q

subarachnoid hemorrhage

A

between arachnoid and pia
2types: non-traumatic, traumatic

CT: blood will bbe seen in contours of brain sulci

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27
Q

non-traumatic subarachnoid hemorrhage

A

rupture of arterial aneurysm
- AVM

R/F: atherosclerotic, blood vesselcongenital abnormalities

Sudden catastrophic headache!

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28
Q

traumatic subarachnoid hemorrhage

A

bleeding into the CSF from damaged vessels due to contusions and other traumatic injuries
- more common than non-traumatic

  • HA iis usually severe due to meningeal irritation from blood in th eCSF
  • deficits are usually related to the presence of other cerebral injuries
29
Q

intracerebral hemorrhage

A
  • occurs within brain parenchyma in cerebral hemispheres, brainstem, cerebellum, or spinal cord

can be traumatic or non-traumatic

30
Q

traumatic intracerebral hemorrhage

A

contusions of cerebral hemispheres occur where cerebral gyri are immediately adjacent to ridges of the skull
-most common at ttemporal and frontal poles

31
Q

non-traumatic intracerebral hemorrhage

A

caused by HTN, brain tumors, secondary hemorrhage after ischemic infarction, vascular malformations, coagulation abnormalities, infections

32
Q

extracranial hemorrhage

A

head trauma can cause:

  • hemorrhage behind the ear drum in the inner ear canal
  • hemorrhage into subcutaneous tissues (raccoon eyes)
  • hemorrhage between external periosteum and galea aponeurotica (goose egg)

need to r/o skull f with all of these injuries

33
Q

closedhead injury

A

occurs when the soft tissue of the brain is forced into contact with the hard, bony skull
- no skull fracture or laceration

34
Q

countercoup injury

A

damage may also occur at the opposite end of the brain suring impact as the brain bounces off the inside of the skull
- usually explains involvement of the brain on opposite sides from one another

35
Q

open head injury

A

occurs when the skull and meninges have been disrupted leaving the brain exposed

36
Q

TBI: secondary damage:

A

refers to the events that occur after the primary or direct damage to the brain tissue
- it is the brains reaction to the trauma

37
Q

secondary damage to vascular changes

A

vascular changes sustained at the moment of impact leads to infarction of the cortical grey matter

  • intercranial hemorrhage causing hypoxia to areas supplied by the hemorrhaging vessels as well as pressure and brain distortion from the collecting fluid
38
Q

secondary axonal injury

A

shear and tensile forces disrupt the axolema which impairs transmission from the cell body and swelling of the axon

  • distal segment will undergo Wallerian degeneration
    • the myelin sheath pulls away from the axon distal to the injury
39
Q

secondary damage: pressure changes

A

dur primarily to lack of oxygen to brain tissue

  • incr ICP resulting from swelling or intercranial hematoma
  • normal ICP : 4-15 mmHg
  • greater than 20 mmHg is associated with increased morbidity
  • monitored in patients with GCS of 7 or less who have an abnormal CT scan
40
Q

secondary damage compression

A

the most common herniation is the lateral tentorial membrane separating from the cerebral hemispheres from the posterior fossa

  • compression of brainstem and others may lead to paralysis
41
Q

secondary damage : perfusion changes

A

intracranial HTN can interfere with perfusion by lowering the cerebral perfusion pressure

  • under normal circumstances cerebral perfusion pressure is maintained at 50-150 mmHg
  • after trauma the CPP can be totally disrupted
42
Q

secondary damage: hypoxia

A

cerebral hypoxia or ischemia occurs when blood vessels are ruptured or compressed, thus depriving the brain of oxygen

  • early hypotension is a strong predictor of a poor outcome
43
Q

thrombophlebitis

A

inflammation of a vein accompanied by a formation of a clot

44
Q

respiratory complication of TBI

A

neurogenic pulmonary edema
aspiration pneumonia
pulmonary emboli

45
Q

cardiovascular complications of TBI

A

neurogenic arrhythmias

neurogenic HTN

46
Q

TBI complication:

Hetertopic ossification

A

abnormal bone growtharound a joint
cause and pathogenesis is unknown
onset is usually 4-12 weeks after the head injury
loss of ROM local tenderness palpable mass

47
Q

cranial nerve damage of TBI

A

the optic nerve is most vulnerable in the optic canal which can result monocular blindness

Occulomotor CNIII

CN IV is the least most common injured with TBI

the trigeminal V is usually involved as they emerge fro supraorbitalarea

CNVI is usually involved when the head is crushed in an anteroposterior plance with lateral expansion of the skull

CN VII is common with injury to temporal bone as wellas CN VIII vestibulocochlear

Cn IX , X, XI can be injured as they pass through the jugular foramen as the base of the skull

48
Q

coma

A

complete paralysis of cerebralfunction; a state of unresponsiveness

  • lowest level of consciousness and is characterized by not following commands,not uttering words, and not opening eyes
  • rarely lasts longer than 4 weeks
49
Q

stupor

A

condition of general unresponsiveness, but can be aroused by repeated heavy stimulus

50
Q

obtundity

A

client who sleeps a lot, when awake has reduced awareness

51
Q

delirium

A

disorientation , fear, misinterpretation of sensory stimuli

52
Q

concussion

A

transient loss of neurologic function in the post head injured period which resolves without permanent gross neurologic sequel or gross neuropathic damage

53
Q

Minor head injury :

post traumatic synrome

A
  • normal CT and neurologic exam
  • significant deficits in detailed neuropsychologic testing
  • headaches, giddiness, easily fatigues, memory deficits, and inability toconcentrate
  • personality changes
  • symptoms worsened with changes in posture, sunlight, heat, exercise, and alcohol ingestion
54
Q

Levels of concussion

grades 1 and 2 AND 3

A
  • no loss on consciousness
    -transient confusion
    -resolution on concussion symptoms or mental status abnormalities occurs :
    Less than 15 min grade 1
    More than 15 min grade 2
    Grade 3 is any loss of consciousness

Grade 2 and 3 should not return to play
Grade 1 may return if sideline neurological exam is normal. multiple grade 1 concussions or grade 2 return in 1 week. Multiple grade 2 or grade 3- with prolonged loss of consciousness return to sport in 2 weeks

55
Q

Major head injury: clinical manifestations

A 
area specific
sensory impairments
abnormal tone
cognitive/behavioral impairment
balance/vestibular/coordination impairments
communication/speech impairment
visual-perceptual impairments
swallowing impairment
56
Q

decorticate posturing

A

hyperactive flexor reflexes in the upper extremities, hyperactive extensor reflexes in the lower extremities (cerebral hemispheres,internal capsule, thalamus)

57
Q

decerebrate posturing

A

hyperactive extensor reflexes in both the upper an lower extremities (brainstem and cerebellum)

58
Q

Glasgow coma scale

A

scored from 3-15. 3 worst
-It is composed of three parameters: Best eye response, best verbal response, best motor response

Observed and recorded on a half hour basis until GCS equal to 15 has been achieved

13-15 - mild head injury
9-12 - moderate head injury
8 or less - coma/ severe head injury

59
Q

retrograde amnesia

A

is the partial or total loss of the ability to recll events that have occurred during the period immediately preceding the head injury

60
Q

posttraumatic amnesia

A

is the time lapse between the injury and the point where memory returns

61
Q

anterograde memory

A

is the ability to form new memory

- loss of anterograde memory is common

62
Q

Rancho levels of cognitive function for traumatic head injury

A 
Level I - no response
Level  II Generalized response
Level II - localized response
Level  IV- confused and agitated 
Level  V confused - inappropriate
Level  VI - confused - appropriate
Level VII- automatic -appropriate
Level VIII purposeful -appropriate
63
Q

Drugs that decrease ICP

A

elevated ICP >20 mmHg is poor prognosis
-cerebral fluid volume can be controlled with mannitol to control blood volume

  • cerebral edema can be treated with Glucocorticoids
  • surgical intervention if a craniotomy is necessary to prevent neurological compromise
64
Q

subacute management of TBI

A

mainatian homeostasis of te hbrain
-control seizures
-control aggressive behavior
prevention of pressure soresand joint contractures
- control of hypertonicity and spasticity

65
Q

GCS Best eye response

A
  • no eye opening
  • eye opening to pain
  • eye opening to verbal command
  • eye open spontaneously
66
Q

GCS Best verbal response

A

No verbal response incomprehensible sounds
inappropriate words
confused
oriented

67
Q

GCS best motor response

A 
no motor response
extension to pain 
flexion to pain 
withdrawal from pain
localizing pain
obeys commands
68
Q

Depth of coma - prognosis GCS

  • within 24 hrs
  • after 24 hrs
A

within
-<8 have a higher mortality rate or risk of a vegetative state
>8 have a very low mortality rate

After 24
< or = 5 is predictive of a poor outcome
>5 is predictive of a good outcome

Neuroscience (6 decks)

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