Week 9: NEUROCOGNITION I Flashcards
Processes
- Sensory input - receive sensory input from the external environment
- Integration – Nervous system processes that input, and decides what should be done
about it - Motor output – the response that occurs when your nervous system activates certain
parts of your brain
Central Nervous System
(main control center)
- Composed of – brain, spinal cord
- Contains – relay neurons (interneurons)
Peripheral Nervous System
(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)
Neurons
- 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
Specialized NS Cells: Neurons
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
Specialized NS Cells: Neuroglia/glial cells
“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
Cerebral Vasculature
- Brain requires perfusion
- Perfused through internal carotid arteries and vertebral arteries
- The further upstream towards the brain the blockage, the bigger the consequences
The Meninges
The Meninges – protective membranes surrounding the brain and spinal cord
- Outer to inner:
o Duramater
o Arachnoid
o Piamater
Cerebrospinal Fluid (CSF)
- Clear, bathes our CNS organs
- Produced by specialized cells
- Stored by carotid plexus (3rd and 4th ventricles)
- Travels through the subarachnoid space
Intracranial Pressure (ICP)
- Pressure within the cranial cavity (ridged bone)
- Measured in mmHg (normal = 5-10mmHg)
- Impacted by volume:
o Brain tissue, blood, CSF
Causes of increased Intracranial pressure
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
Nursing assessment: Intracranial Pressure
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
Labs and investigations: Intracranial pressure
CT/MRI – visualize the ventricles and brain tissues (can see damage)
Nursing management: Intracranial pressure
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
Cushing’s Triad
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!
CPP = MAP – ICP
- 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
Brainstem Herniation
- 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)
Stages of Brain Herniation
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)
Spinal Cord Injury (SCI)
- 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
Classifications: Spinal cord injury
Complete transection
Complete loss of mobility, sensation, reflexes (100%)
Incomplete/partial transection
Some signals, movement and retention is retained
Paraplegia
lower extremity
Tetraplegia (quadriplegia)
all extremities
Level of injury: Spinal cord injury
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
Brown-Sequard Syndrome
Partial transection of one half of the spinal cord
One outcome on one side of body, one outcome on other side (contralateral)
Central Cord Syndrome
Can cause damage to different parts of body
Posterior Cord Syndrome/Anterior Cord Syndrome
Might see damage to only one type of nervous function
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
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
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
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?
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
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
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