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Nursing 3910 > Week 9: NEUROCOGNITION I > Flashcards

Week 9: NEUROCOGNITION I Flashcards

1
Q

Processes

A
  1. Sensory input - receive sensory input from the external environment
  2. Integration – Nervous system processes that input, and decides what should be done
    about it
  3. Motor output – the response that occurs when your nervous system activates certain
    parts of your brain
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2
Q

Central Nervous System

A

(main control center)

  • Composed of – brain, spinal cord
  • Contains – relay neurons (interneurons)
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3
Q

Peripheral Nervous System

A

(allow central nervous system to communicate with the rest of the body)

  • Composed of – cranial nerves, spinal nerves, peripheral nerves
  • Contains:
    Sensory (afferent) neurons

Motor (efferent) neurons:
 Somatic NS – voluntary
 Autonomic NS – involuntary
 Sympathetic (fight or flight), parasympathetic (rest and digest)

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4
Q

Neurons

A
  • Nerve cells in the brain and nervous system
  • Structure:
    o Cell body – contains organelles
    o Dendrites – receive signals and convey information to the cell body
    o Axon – transmit electrical impulses away from the cell body to other cells
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5
Q

Specialized NS Cells: Neurons

A

Neurons - respond to stimuli and transmit signals

o Sensory (afferent) – transmit impulses from sensory receptors toward the CNS

o Motor (efferent) – impulse moves from the CNS to the rest of the body, mostly multipolar

o Interneurons (association) – impulse moves between sensory and motor neurons

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6
Q

Specialized NS Cells: Neuroglia/glial cells

A

“Glue”

Provide support, nutrition, insulation, and help with signal transmission.

CNS:
 Astrocytes – exchange of materials between neurons and capillaries
 Microglial – immune defence against invading microorganisms
 Ependymal–line cavities; create, secrete and circulate CSF
 Oligodendrocytes – wrap and insulate, form myelin sheath

PNS:
 Satellite – surround and support neuron cell bodies
 Schwann – insulate, help form myelin sheath

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7
Q

Cerebral Vasculature

A
  • Brain requires perfusion
  • Perfused through internal carotid arteries and vertebral arteries
  • The further upstream towards the brain the blockage, the bigger the consequences
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8
Q

The Meninges

A

The Meninges – protective membranes surrounding the brain and spinal cord

  • Outer to inner:
    o Duramater
    o Arachnoid
    o Piamater
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9
Q

Cerebrospinal Fluid (CSF)

A
  • Clear, bathes our CNS organs
  • Produced by specialized cells
  • Stored by carotid plexus (3rd and 4th ventricles)
  • Travels through the subarachnoid space
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10
Q

Intracranial Pressure (ICP)

A
  • Pressure within the cranial cavity (ridged bone)
  • Measured in mmHg (normal = 5-10mmHg)
  • Impacted by volume:
    o Brain tissue, blood, CSF
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11
Q

Causes of increased Intracranial pressure

A

o Stroke
o Infection – meningitis, encephalitis
o Trauma, aneurysms
o Hypertension – causes change in MAP
o Hypoxemia – inadequate O2 levels, increased CO2 levels in brain o Tumours – space occupying
o Hydrocephalus
o Seizures/epilepsy

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12
Q

Nursing assessment: Intracranial Pressure

A

Health history:
 Any risk factors?
 Headache, nuchal rigidity, blurred vision, changes in LOC
 Early recognition is important!!

Physical assessment:
 Weakness
 Nausea/vomiting (lots, rapid onset)
 Pupil changes/no blinking
 Ataxia, coordination issues
 Seizure
 Hemodynamic instability (increased bp, decreased hr)
 Respiratory distress
 Cushing’s triad

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13
Q

Labs and investigations: Intracranial pressure

A

CT/MRI – visualize the ventricles and brain tissues (can see damage)

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14
Q

Nursing management: Intracranial pressure

A

Peak edema = 3-5 days afer injury
- Monitor ABCs
- Frequent neuro assessments
- Elevate head of bed – 30 degrees, decrease stimuli

  • Administer IV hypertonic solutions to decrease cerebral edema (20% mannitol,
    3% normal saline)
  • Initiate feeding early – brain has high metabolism, requires lots of protein to heal
  • Medical interventions – lower pressure
  • VP or LP shunts
  • Change vent settings – hyperventilation
  • Sx – craniectomy
  • Meds – acetazolamide
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15
Q

Cushing’s Triad

A

Late-stage symptom of ICP – close to brainstem herniation

Body’s attempt to save brain tissue during severe lowered perfusion

Bradycardia, low, irregular respirations, hypertension** needs emergent medical
attention!

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16
Q

CPP = MAP – ICP

A
  • MAP = 70-100mmHg
  • Blood pressure during a cardiac cycle
  • Cerebral Perfusion Pressure (CPP) = 60-80mmHg
  • Pressure gradient that drives oxygen delivery to cerebral tissue
  • Maintaining normal CPP is vital to ensure that the brain receives enough oxygen
  • Increased ICP = decreased CPP = brain ischemia = brain damage and death
17
Q

Brainstem Herniation

A
  • Brainstem begins to protrude out of cranial cavity and into spinal cord
  • Brainstem is responsible for lots of autonomic body processes (eg. Breathing)
  • Causes the loss of ability to engage in essential body functioning
  • Patients become very ill, very quickly
  • Cushing’s triad, oculocephalic reflex (eyes do not follow when turning head), babinski’s
    reflex (toes fan up when bottom of foot is stimulated, not down)
18
Q

Stages of Brain Herniation

A

o Obey commands
o Bilateral Babinski’s reflex
o Hypertonia (cannot relax muscles)
o Grasp reflex
o Decorticate
o Decerebrate
o Flaccidity (no motor response to painful stimuli)

19
Q

Spinal Cord Injury (SCI)

A
  • Damage to the spinal cord resulting in physiologic impacts on strength, motor function,
    bladder/bower function, sensation, reflexes, etc.
  • Temporary or permanent
  • Damage depends on extent and location of injury
  • Injury progression:
    o Primary injury – initial traumatic event/insult
    o Secondary injury – edema and hemorrhage that follows the injury, early intervention prevents further damage
  • Prognosis most accurately assessed 72+ hours post trauma – period in which edema/bleeding (hopefully) subsides
  • Traumatic cause:
    o MVA, fall, sports, violence
  • Non-traumatic cause:
    o Tumour, inflammation, infection
  • Highest risk: men 16-30
20
Q

Classifications: Spinal cord injury

A

Complete transection
 Complete loss of mobility, sensation, reflexes (100%)

Incomplete/partial transection
 Some signals, movement and retention is retained

21
Q

Paraplegia

A

lower extremity

22
Q

Tetraplegia (quadriplegia)

A

all extremities

23
Q

Level of injury: Spinal cord injury

A

Cervical (C1-C8)
 All limbs are affected
 C4 and above: diaphragm, bowel/bladder support

Thoracic (T1-T12)
 Paraplegia
 Control of upper extremeties and trunk

Lumbar (L1-L5)
 Ambulation with assistance
 Hips and legs

Sacral (S1-S5)
 Ambulation with or without assistance

24
Q

Brown-Sequard Syndrome

A

Partial transection of one half of the spinal cord

One outcome on one side of body, one outcome on other side (contralateral)

25
Q

Central Cord Syndrome

A

Can cause damage to different parts of body

26
Q

Posterior Cord Syndrome/Anterior Cord Syndrome

A

Might see damage to only one type of nervous function

27
Q

Systemic Impacts: Spinal Cord Injury

A

Respiratory
- Function of accessory muscles and diaphragm
- Mechanical ventilation
- Poor muscle control – hypoventilation, atelectasis, pneumonia

CV
- SNS activation can be compromised, causing bradycardia, vasodilation,
hypotension, decreased CO
- DVT

Pain
Thermoregulation

Urinary
- Retention

GI
- Hypomobility
- Bowel reflexivity

Integumentary
- Skin breakdown risk

Musculoskeletal
- Range of motion
- Atrophy

28
Q

Emergency Nursing Management: SCI

A

Immobilize
Lay flat, log roll
No twisting, turning or sitting
Apply immobility devices – board, cervical collar, halo

ABCs
 Patent airway, supplement O2
 Treat shock
 Support perfusion (support fluid volume, control hemorrhage)

o Pain management

29
Q

SCI Complications: Autonomic Dysreflexia

A

Autonomic Dysreflexia

ONLY above T6

Caused by stimulation of sensory receptors below injury – causes
vasoconstriction and HTN – body cannot properly interpret and respond to stimulus

30
Q

Signs and symptoms of SCI complications: Autonomic Dysreflexia

A

 Pounding/throbbing headache
 HTN, bradycardia
 Sweating/flushing above site of injury
 Goosebumps (piloerection)
 Nasal congestion

Nurse management:
 Notify MRP
 HOB 45 degrees
 Administer antihypertensives (IV)
 Assess GI/GU – catheter, infection, overfull bladder?

31
Q

SCI Complications: Spinal Shock

A

Occurs immediately post-SCI – presents as quadriplegic, will resolve in 72 hour
period

Areflexia – motor, bladder, bowel

Loss of sensation, paralysis, flaccidity

Vital signs: bradycardia, hypotension

Can be caused by excessive inflammation

Causes:
 Hypovolemic (hemorrhage)
 Cardiogenic (MI)
 Distributive
–Neurogenic – SCI
–Anaphylactic – severe allergic reaction
–Septic – systemic infection

32
Q

SCI Complications: Neurogenic shock

A

No cardiac compensation

Causes:
- Autonomic dysfunction – decreased systemic vascular resistance and
bradycardia – vasodilation and venous pooling

Presentation:
- Abrupt fever and perspiration above injury
- Warm, dry skin below injury
- Bradycardia, severe hypotension

Nursing management:
- Notify rapid response (code blue)
 ABCs
 Administer O2
 IV access
 Administer IV vasopressors
 Administer IV Atropine for bradycardia
 Document CODE

33
Q
A

Nursing 3910 (12 decks)

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