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
Central Cord Syndrome
Can cause damage to different parts of body
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Posterior Cord Syndrome/Anterior Cord Syndrome
Might see damage to only one type of nervous function
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Systemic Impacts: Spinal Cord Injury
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
Emergency Nursing Management: SCI
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
SCI Complications: Autonomic Dysreflexia
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
Signs and symptoms of SCI complications: Autonomic Dysreflexia
 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
SCI Complications: Spinal Shock
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
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SCI Complications: Neurogenic shock
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
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