Cognition

Book Notes

A. Brain Trauma

a. Traumatic Brain injury

i. Cause: Motor vehicle collisions, falls, firearms, assaults, sportsrelated trauma, recreational injuries, and war-related injuries.
ii. Risks:
1. substance abuse, not wearing seatbelt or helmet, accidental
injuries, violence
iii. Classificationsdetermined by GCS
1. Primary- occurs immediately on impact of mechanical force
a. Damage to brain or vasculature is done and cant be
reversed.
b. EX. Contusion, penetration, hematoma, Intracerebral
hematoma
2. Secondary- evolves over next hours or days (swelling of brain)
a. Result of inadequate nutrients and oxygen to brain cells
b. Decreased perfusion, hypoxia, infection, electrolyte
imbalance contribute to secondary
iv. Types:
1. Scalp laceration- easily recognized, major complication is
bleeding and infection
a. Manifestation: profuse bleeding
2. Skull fractures linear or depressed, simple, comminuted or
compound, and closed or open
a. Manifestations: location determines the manifestations.
Battles sign (behind the ear ecchymosis) and periorbital
ecchymosis (raccoon eyes) Rhinorrhea (CSF leakage from
nose) otorrhea (CSF leakage from ear)

b.
c. Complication: intracranial infection (meningitis), hematoma,
meningeal and brain tissue damage.
d. S&S:
i. Mild injury
1. Loss of consciousness for a few seconds to a few
minutes, no loss of consciousness (but is dazed and
confused), memory/ concentration problems,
headache, dizzy/ loss of balance, N/V, ringing in
ears, sensitive to light, mood change, depressed,
fatigue, difficulty sleeping, sleep more than usual
ii. Moderate injury
1. Loss of conscious for several hours, profound
confused, agitation/ combative, unable to awaken
from sleep, slurred speech, weak or numb
fingers/toes, persistent headache, repeated
vomiting, dilation of one or both pupils in eyes,
clear fluid draining from nose or ears
iii. Children
1. Change in eating/ nursing habit, persistent crying,
unusual irritability, change in ability to pay
attention, change in sleeping habits, sad/depressed
mood, loss of interest
e. Diagnostic:
i. GCS, CAT scan, MRI, SPECT scan, PET scan, Ranchos Los
Amigos scale, evaluation from physicians
f. Testing: determine whether the fluid leaking from nose or
ear.

i. Test fluid with Dextrostix or Tes-Tape strip to determine

whether glucose is present. CSF give a positive reading
in glucose
ii. If blood present in the fluid than test is not reliable.
Allow the leaking fluid to drip onto a gauze pad and
observe the drainage. Blood should coalesce in the
center and yellowish ring encircles the blood if CSF if
present also known as Halo/Target sign.
g. Treatment
h. Interventions
i. Primary Prevention: educating about safety and disease
prevention. Wear helmets and seatbelts
ii. Secondary prevention: screening and diagnosis of injury.
1. Keep pt. oxygenated and allow for perfusion
2. Stay talking to patient for neuro assessment
throughout shift
3. Keep patient on fall risk
iii. Tertiary prevention: occupation therapy or rehabilitation
to bring patient back to best state of health
b. Head trauma (pg 1372 Table 57-9 show interventions)
i. Types:
1. Diffuse injury (Generalized)
a. Concussion: sudden transient mechanical head injury with
disruption of neural activity and a change in LOC
i. Cause: rapid acceleration-deceleration or sharp blow to
head
ii. S&S: altered LOC, amnesia regarding then even, and
headache. May lose conscious or not loss conscious and
typically short lived.
b. DAI(diffuse axonal injury): widespread axonal damage after
a mild, moderate, or severe TBI
i. Cause: tearing, shearing, strains and compression of
axons in the brain
ii. S&S: decreased LOC, increased ICP, global cerebral
edema, immediate prolonged coma longer than 6 hrs,
decorticate/decerebrate positons
2. Focal Injury (localized)
a. Can be minor to severe. Localized to an area of injury.
Consist of lacerations, contusions, hematomas, and cranial
nerve injuries
b. Lacerations: actual tearing of the brain tissue
i. S&S: if severe hemorrhage, hematoma formation,
seizures, and cerebral edema. Unconsciousness,
hemiplegia on contralateral side, and dilated pupil on
ipsilateral side.
ii. Treatment: antibiotics until meningitis is ruled out
c. Contusion: bruising of brain tissue within a focal area.
i. S&S: may have hemorrhage, infarction, necrosis, and
edema
1. Increased bleeding if taking anticoagulants

ii.
iii.

iv.

v.

2. Coup-countrecoup injury: brain moves inside the

skull due to high-energy causing contusion on the
skull/brain and a secondary area of damage on the
opposite side away
from injury.
d. Epidural Hematoma: bleeding
between the dura and the inner
surface of the skull. (can be
arterial or venous and typically
faster death)
i. S&S: initial period of
unconsciousness,
decreased LOC, headache,
N/V, focal findings
ii. Treatment: surgical
intervention, cerebral
herniation, medical management of increased ICP
e. Intracerebral/subarachnoid hematoma- hemorrhage into
brain tissue
f. Subdural Hematoma: bleeding between the dura mater and
the arachnoid layer of the meninges (venous and typically
slower)Can be acute or chronic and occur w/I 48 hrs.
i. S&S: increased ICP, decreased LOC, & headache. May be
drowsy and confused to unconscious, pupil dilations
ii. Treatment: craniotomy, evacuation and decompression,
membranecotomy (all depend on severity)
Diagnostic test:
1. CT, MRI, PET, X-ray of head and neck, Angiography
Assessment:
1. Altered LOC, confusion, altered respiration, pupil abnormalities,
altered gag reflex, sudden onset of neurological deficit, change
in vitals (increased or decreased temp, Cheyne- Stroke
Respirations, bradycardia, increased BP), vision/ hearing
impaired, sensory dysfunction, motor response, headache,
seizures, N/V (severe if projectile), mental status change
Treatment:
1. Concussion and contusion: observe and manage increased ICP
2. Skull fracture: craniotomy and cranioplasty will be needed
3. Hematomas: blood must be removed and a craniotomy is
generally performed
Interventions:
1. Maintain adequate cerebral oxygenation, remain normothermic,
achieve control of pain and discomfort, be free form infection,
have adequate nutrition, and attain maximal cognitive, motor,
and sensory function.
2. Endotracheal intubation and ventilator support may be
necessary
3. Teaching: Table 57-11 pg. 1374
a. NO: drinking, driving, use of fire arms, working w/ hazardous
machinery, unsupervised smoking

vi. Post
1.
2.
3.
4.
5.

surgical:
Flat or slight elevate (10-15o) for post op phase. 30o after
Avoid phenogran as anti-seizure medication
Monitor F&E, DI, and hypovolemic shock
Dressing will be wrapped around head
If craniectomy do not place pt on the side of operation

B. Encephalopathy
a. Definition:
i. Related more to an infection in which patient experiences alteration
in mental status
b. Cause:
i. It is multifactorial and includes infection, alcoholism, liver/kidney
problems, change in ICP, poor nutrition, anoxic injury, neurotoxic
effects of ammonia, metabolic diseases, brain tumors, abnormal
neurotransmission, certain medications
c. Grading scale (Table 44-11 pg. 1021)

d. Risks
i. Placement of transjugular intrahepatic portosystemic shunt (TIPS), GI
hemorrhage, constipation, hypokalemia, hypovolemia, infection,
cerebral depressant, metabolic alkalosis, paracentesis, dehydration,
increase metabolism, uremia
e. Manifestations
i. Could be sudden or slow changes
ii. Asterixis (flapping tremors), apraxia(inability to construct simple
figures w/ pen), fetor hepaticus (musty/sweet odor of patients
breath), Change in neuro and mental responsiveness, impaired
consciousness, inappropriate behavior, lethargy/ sleep disturbance,
nervousness, forgetful, disturbed sleep pattern.
iii. if caused by infection they will have fever, headache, Nausea,
seizures, abnormal cerebrospinal fluid
f. Diagnostic study
i. Mental status test, memory tests, coordination tests
g. Treatment
i. Treat precipitating causes.

1. Control GI bleeding and removing the blood from GI tract if

caused from hepatic conditions
h. Interventions
i. Medications
1. Antibiotics (rifaximin[xifaxan])
2. Lactulose (Cephulac)
ii. Keep them on a protein restricted diet unless they have persistent
hepatic encephalopathy. Only necessary if it is episodic hepatic
encephalopathy.
iii. Asses neuro status every 2 hrs,
iv. Prevent constipation and reduce ammonia production.
v. Encourage fluids if not a contraindication but focus on preventing
fluid loss such as diarrhea and hypovolemia.
vi. Prevent the use of opioid medications because it could worsen the
condition.
vii. Monitor O2, cap refill, and orientation X3

C. Postpartum Psychosis
a. Definition:
i. Is very rare but is a psychiatric emergency. Is considered an overt
presentation of bipolar disorder after delivery
b. Etiology
i. Once a mother has had an episode of postpartum psychosis, she has
a 30-50% change of recurrence after the next birth.
c. S&S
i. Typically shows w/I 2 wks postpartum.
ii. Patient may have auditory or visual hallucinations, paranoid or
grandiose delusions, elements of delirium or disorientation, and
extreme deficit in judgment accompanied by high levels of
impulsivity that may increase risk of suicide of infanticide
iii. Typically begins with fatigue, insomnia, and restlessness. May have
episodes of tearfulness and emotional lability
iv. Complaints of inability to move, stand, or work
v. Later on may feel confused, incoherence, irrational statements, OCD
about baby
d. Treatment
i. Medications
1. Lithium, Antipsychotics, Mood stabilizers,
Benzodiazepines
2. Antidepressants
a. Should be used with caution due to risk of precipitating
rapid cycling
ii. ECT and Psychotherapy are other options
e. Interventions
i. Inform about the risks of breastfeeding and taking medications
ii. Safety risk for infant and mother!
iii. Outpatient follow-up care is critical and timely remission of symptoms
is important so mother can bond with infant
iv. Arrange for family, friend, and professional support os mother can
get sleep and recover

v. Monitor for medication side effects

D. Schizophrenia
a. Definition
i. A brain disorder that affects a persons thinking, language, emotions,
social behavior, and ability to perceive reality accurately.
1. Chronic, severe, and disability brain disorder
2. It appears in late teens and early twenties
b. Comorbidity
i. Substance abuse, anxiety/depression/suicide, hypertension, obesity,
cardiovascular disease, diabetes, COPD, trauma, polydipsia,
stressors, genetics
c. Phases
i. Phase I- onset or exacerbation f disruptive symptoms w/ result of loss
of functional abilities
ii. Phase II- symptoms diminishing, no movement toward ones previous
level of function. Partial hospitalization
iii. Phase III- patient is near or at baseline. Symptoms are absent or
diminished; level of functioning allows the pt. to live in community.
d. Cause
i. Genetics, high dopamine and serotonin levels, enlargement of brain
ventricles, reduced cortical/frontal lobes, increased fissure size,
environmental and psychological stressors,
e. S&S
i. Will initially be socially awkward, lonely, depressed, vague expression
of self.
ii. Will then experience anxiety, phobias, obsession, dissociation, and
compulsions
iii. Finally will have mind wondering, incompletion of school or job
related work, memory/ concentration destroyed
f. Treatment
i. Psychiatrist and psychopharmacology
1. Typically older meds like... Haldol, thoazine, prolixin but can
be newer meds like.
2. Clozaril, Risperdal, Zyprexa, Seroquel, abilify, invega,
Geodon, latuda
g. Interventions
i. Provide support, psychoeducation, and guidance
ii. Safety is key!!!!