1. Gerontological Nursing
COGNITIVE AND
NEUROLOGICAL FUNCTION
Jose Karlo M. Pañgan,RN, MAN
`
Week
NINE

2. CENTRAL NERVOUS
SYSTEM (CNS)
Brain
Spinal Cord
PERIPHERAL
NERVOUS SYSTEM
Cranial Nerves
Spinal Nerves
Somatic Nervous
System
Autonomic Nervous
System
Reflex Arc

5. Neuron
Shrinkage in neuron size and
gradual decrease in neuron
numbers.
Structural changes in dendrites.
Deposits of lipofuscin
granules, neuritic plaque and
neurofibrillary bodies within
cytoplasm and neuron.
Loss of myelin and decreased
conduction

8. Changes in precursors
necessary for
neurotransmitter
synthesis.
Change in receptor sites.
Alteration in enzymes
that synthesize and
degrade
neurotransmitters
Significant decrease in
neurotransmitter.

9. Motor
Muscular atrophy
– decrease in
muscle bulk
Decrease in
electrical
conduction
system

10. Decrease in electrical
conduction
Atrophy of taste buds
Alteration in olfactory
nerve fibers
Alteration in nerve cells of
vestibular system of inner
ear, cerebellum, and
proprioception.

11. Altered electrical
conduction of the
nerve due to
myelin loss
Altered reflexes
response
(ankle, superficial
reflexes

12. Disruption of
stage 3 and 4 of
the sleep cycle

13. Stages Type of Sleep Selected Characteristics
NON-REM SLEEP (4 STAGES)
STAGE 1 LIGHT SLEEP EASILY AWAKENED
STAGE 2 MEDIUM DEEP SLEEP MORE RELAXED
SLOW EYE MOVEMENTS
FRAGMENT DREAMS
EASILY AWAKENED
STAGE 3 MEDIUM DEEP SLEEP RELAXED MUSCLES
SLOWED MUSCLE
DEC. TEMP
AWAKENED BY MOD.STIMULI
STAGE 4 DEEP SLEEP RESTORATIVE SLEEP
RARE BODY MOVEMENT
AWAKENED BY VIGOROUS STIMULI
REM ACTIVE SLEEP REM
INCREASED OR FLUCTUATING PULSE,
BP, RR
DREAMING

14. Slowing of
autonomic nervous
system response as
a result of
structural changes
in basal ganglia.

15. Reduction in the
turnover of CSF.

17. Most common mental
disorder in the older adults.
Between the ages of 80 and
84, 17% of men and 22% of
women have severe
depression.
By age 85, the percentage of
older persons with depressive
symptoms equalizes.
Not a normal consequence of
aging.
A significant risk for suicide.

18. Changes in feelings or
mood, described as
feeling
sad, hopeless, pessimistic
or “blue” lasting most of
the day.
Fatigue, constipation, psy
chomotor
retardation, depressed
mood, loss of
interest, energy, libido or
pleasure, changes in
appetite, weight and
sleeping pattern.

19. Common response to serious illness of any kind
(MS, hypothyroidism, SLE, Hepatitis, AIDS, anem
ia)
Drugs
(Amphetamines, analgesics, narcotics, anti
HPN, anti-microbials, anti-Neoplastics, anti-
parkinsonian, barbiturates, benzodiazepines, dig
oxin, hypoglycemics, phenothizides, steroids, sul
fonamides)

20. PSEUDODEMENTIA
– depression
masquerading as
DEMENTIA
PSEUDODELIRIUM
– term used when
an older adult is
seem to be with an
acute confusion
found to be due to
depression.

21. Anti-depressants
 Trazodone
 First line of treatment
 Mild to moderate agitation
 25-50 mg
 SSRI
 Paroxetine (Paxil), Sertraline
(Zoloft), and Fluoxetine (Prozac) –
agitation.
 Benzodiazepine – reserved for acute
conditions
 Lorazepam (Ativan) – 0.25 mg to 1 mg
orally or IM
 Oxazepam – 5-10 mg
 Buspirone – anxiety triggered agitation
 Anti-epileptic Or Anti-convulsants
 Carbamazepine (tegretol) 4-8 mcg/ml
 Valproic acid

22. Transient, organic
mental syndrome
characterized by
reduced level of
consciousness, reduc
ed ability to
maintain
attention, perceptua
l disturbances and
memory
impairment.

23. ONSET: Short (hours to
days)
LOCATION: occur in all
areas (frequently
precipitates hospital
admission)
RISK FACTORS:
Advanced age, CNS
diseases, infection, polypharma
cy, GIT, GUT, CPD sensory
changes

24.  Medical conditions that
causes Delirium
IN THE BRAIN –
stroke, trauma, meningi
tis, and vascular
disorder.
OUT THE BRAIN –
endocrine
dysfunction, organ
failure, infections, meta
bolic
disorders, shock, burns,
dehydration, and
nutritional deficiency.

25. MEDICATIONS
IN THE BODY –
opiates, anticholinergic
medications, steroids, p
sychoactive drugs, OTC
cold drug preparations.
OUT THE BODY –
alcohol
withdrawal, steroid
withdrawal, SSRI
withdrawal.

26. Change: Recent onset and
fluctuate during the
course of the day.
Difficulty maintaining
concentration or attention
to external stimuli
Language disturbance
(slurred, forced or
rambling speech)
Disorganized thinking
(tangenital reasoning and
conversation)
Disturbances of
consciousness.
Change in cognition

27. Early assessment
Delirium rating scale
Delirium symptom
interview
Identification of risk
factors
Delirium, visual
impairments, severe
illness, cognitive
impairments and high
BUN and Creatinine.

28.  NON-PHARMACOLOGIC
INTERVENTION
 Removing bladder catheters
 Improving nutritional intake
 Providing reality orientation
PHARMACOLOGIC
 Decreasing sensory
overstimulation or deprivation
AND NON
PHARMACOLOGIC
 Reassuring the older adult and
his or her family members. INTERVENTIONS
 PHARMACOLOGIC
 Agitations and hallucination –
Haloperidol
 Alcohol withdrawal symptoms
– benzodiazepines

29. Is a syndrome of gradual and
progressive cognitive decline
Alteration in memory
Characterized by a loss of
cognition and at least one of the
following
 Ability to speak coherently and understand
language (APHASIA)
 Ability to recognize or identify objects
(AGNOSIA)
 Ability to execute motor activities
(APRAXIA)
 Ability to think abstractly, make sound
judgment, and plan and carry out complex
tasks

30. Phenomenon that occurs when
other pathologic condition
masquerade as dementia.
Medications, ethyl alcohol
intoxication or
withdrawal, metabolic disorders
(thyroid disorders, Vitamin
B12, hyponatremia, hypercalcemi
a, hepatic and renal dysfunction)
depression, delirium, CNS
neoplasms, chronic subdural
hematoma, normal pressure
hydrocephalus.

31. Progressive
neurodegenerative disease
characterized by the
presence of neurofibrillary
tangles composed of
misplaced proteins within
the brain, cortical amyloid
plaques, and
granulovascular
degeneration of neurons in
the pyramidal cell layer of
the hippocampus.

32. Genetics
Viral
Age
Head injury
Environmental
exposures
Nutritional
factors

33. Individual’s repeated questions
and statements
Forgetfulness
Increasing problem with
orientation and geographic
disorientation
Memory loss
Language deterioration
Impaired ability to mentally
manipulate visual information
Poor judgment
Confusion
Restlessness
Mood swings
Personality changes

34. MRI
PET

35. No cure for AD
Cognex
 Cholinesterase inhibitors
 Monitor the patient’s liver
Donepezil (Aricept)
Rivastigmine
Galantamine (Reminyl)
Gingko Biloba – herbal plant
extract
 Enhances the cognitive
performance
 Vitamin supplementation

36. Preserving the
dignity and
promoting
independence
Maintaining the
cognitive and global
function early in the
disease process.

37. Loss of cognitive function
resulting from
ischemic, hypoperfusive or
hemorrhagic brain lesions
from a CVD
Abrupt onset of dementia
Multi infarct dementia
(Multiple strokes in CT or MRI
present)
Focal neurological findings
Low-density areas indicate
vascular changes in white
matter
Unchanged personality
Emotional problem

38. Arteriosclerosis, blood
dyscrasias, cardiac
decompensation, hypert
ension, atrial
fibrillation, cardiac valve
replacement, systemic
emboli.

39. Symptoms depends
on the location of the
infarct
 Impaired learning and
impaired retention of
new information
 Impaired handling new
tasks
 Impaired reasoning
ability
 Impaired spatial ability
and orientation
 Impaired language.

40. CT Scan and
MRI

41. Donepezil –
improving
cognition and
function, clinical
global impression
and ability to
perform ADLs.
Nimodipine – short
term benefit for
VAD

42.  Clinical features persist over long
period of time resulting in severe
dementia
 Lewy bodies and Lewy neuritis found
in brain structures
 Found in the Lewy
brainstem, diencephalon, basal
ganglia and cerebral cortex
body
 Lewy bodies : are abnormal dementia
aggregates of protein that develop
inside nerve cells in Parkinson's
disease (PD) and Alzheimer's disease
(AD) and some other disorders.

43. advanced age
Depression
confusion or psychosis
while taking levodopa,
facial masking of individuals
with PD

44. Prominent
fluctuations in
attention and ability
to communicate.
More visual-spatial
processing
impairments and Clinical
subcortical
dementia.
manifestations:
EPS:
rigidity, bradykinesia,
flexed
posture, shuffling
gait.

45. Symptomatic
relief
Cholinesterase
MANAGEMENT:
inhibitors

46. Presence of
frontal brain Fronto-temporal
area atrophy in lobe dementia
CT or MRI

47. Clinical Manifestations:
Frontal or aphasic
variants – changes in
personality and social
cognition, disinhibition
s, loss of Diagnostics – CT
empathy, changes in scan or MRI
eating
pattern, stereotypic
behavior.
Fluent or non fluent
aphasia.

48. Management
3-10 years
No specific
treatment

50. Assessment
Glasgow coma
scale
Mental status
examination
Pupil
examination
Neurologic
assessment
Behavioral
assessment

51. Individualized care for
each patients
Monitor and maintain
physical health
Adapt the environment
Communicate in a
simple, direct manner
Provide cues for reality
orientation
Maintain social interaction
and self esteem.

52. Sundowning
syndrome
Wandering
Paranoia and
suspiciousness
Hallucinations and
Delusions
Catastrophic
Reactions
Resources

54. Primary cause:
Unknown
Other causes: viral
infection, disequilib
rium between
dopamine and
acetylcholine, ence
phalitis, arterioscler
osis, and carbon
monoxide
poisoning, stroke, i
nfections.

55. Tremors
pillrolling tremors
Resting tremors
Cogwheel rigidity
Bradykinesia, Akinesia
Propulsive gait ( begins
walking, then starts running
forward unable to stop until he or
she falls or runs into something.)
Festinating gait ( small steps)
Retropulsion ( walking and falling
backward)

56. Freezing (a phenomenon
where the individual
appears to be glued to the
floor.)
Mask like facial expression
(flat affect)
Emotional
lability, depression
Fatigue
Soft, monotonous voice
Shaky small handwriting
Excessive
sweating, seborrhea, lacri
mation, constipation, decre
ased sexual activity.

57. Diagnostics
EEG
Symptoms
improve with
antiparkinsonian
drugs

58. Aimed: relieving clinical
manifestations, increasing
individual’s ability to
perform ADL’s and
decreasing the risk for
injury.
MEDICATIONS
Anticholinergics
Cogentin (Benztropine)
Akineton (Biperiden)
Artane (Trihexyphenidyl)
 MAO
 Dopaminergics

59.  Monitor v/s, urine output and
bowel sounds
 Observe for involuntary
movements
 Advise the client to avoid Nursing
alcohol, cigarette, caffeine and
aspirin. Intervention for
 Prevent and relieve side effects: the
 Dry mouth : hard candy, ice pharmacologic
chips, sugarless chewing gum
 Photophobia: sunglasses
management:
 Urinary retention: void before
taking the drug
 Increased intraocular pressure:
routine eye examinations

60.  Levodopa
 Carbidopa with Levodopa (Sinemet)
 Nursing Interventions:
 Side effect: Orthostatic Hypotension
 Monitor client’s vital signs and ECG
 Check for weakness, dizziness or
syncope.
 Advise the client to practice
gradual change of position.
 Reddish brown urine and
perspiration
 Harmless but clothes may be
stained.
 Impaired voluntary movement –
takes weeks or months to be
controlled.

61.  Symmetrel (Amantadine HCL) -
dopaminergic
 Parlodel (Bromocriptine
Mesylate)
 Requip (Ropinizole HCL)
 Nursing Interventions:
 Report signs of skin
lesion, seizure or depression.
 Report lightedness when
changing positions.
 Avoid alcohol
 Advise the client not to
abruptly stop the drug
without notifying the health
care provider.

62. Ablation
(destruction)
Deep brain
stimulation
Transplantation

63.  Provide a safe
environment
 Provide measures to
increase mobility:
 Physical therapy, Assistive
devices
 Encourage independence
in self care activities.
 Improve communication
abilities.
 Maintain Adequate
Nutrition
 Avoid constipation and
maintain adequate bowel
elimination.

65. Vision
Lose of tone of the eye
lids and become lax –
ptosis of the
eyelids, redundancy of
the skin, and
malposition of the
eyelids.
Conjunctiva – thins and
yellow in appearance.

66. Sclera – develop brown
spots
 Arcus senilis – surrounding rings
made up of fat deposits at the
cornea.
 Pupil – decrease in size and loses
some of its ability to constrict.
 Limit the amount of light
entering the eye.
Lens – increases in rigidity
and density affecting the
eye’s ability to transmit
and focus light.

67. Peripheral vision
decreases, night vision
diminishes and sensitivity to
glare increases.
Difficulty in identifying cool
colors: blue, green and violet.
Vitreous humor loses
transparency and increases the
scattering of light. (causes
Floaters- dots, wigly lines or
clouds)
Flashers – jagged lines; vit.
Fluid rubs eyes or pulls retina.

68. Decline in the
visual acuity
Presbyopia –
inability to focus
nearby objects.

70. Group of
degenerative eye
diseases in which
the optic nerve is
damaged by high
intraocular
pressure (IOP)
resulting in
blindness due to
nerve atrophy.

71. Race (African
Americans, Asian
American and
Alaska Natives)
eye trauma
small cornea
small anterior
chamber
Family history
Cataracts
Some
Medications

72. Cause:
Unknown, results
from a papillary
blockage that
limits the flow of
aqueous humor
causing an
increase in IOP.

73. More
common, occurs
gradually.
90% of all primary
glaucoma
Degenerative
changes in
Schlemm’s canal
obstruct the escape
of aqueous humor.

74. Peripheral vision loss
gradually and
painlessly
Tired eyes
Seing Halos around
lights
Worse symptoms
experience in the
morning.

75. Symptoms associated with Stress
Medical emergency and the
patient should seek emergency
help immediately.
Severe eye pain in one eye
red eye
Blurred vision
Nausea and Vomiting
Seeing colored halos around the
lights
Bradycardia
Pupil dilation
Steamy appearance of cornea

76. When drainage
angle is damage by
eye injury or other
specific conditions.
Medications
(steroids), tumors, in
flammation, or
abnormal blood
vessels.

77. Diagnosis:
Gonioscopy –
direct exam
Tonometer –
to measure
IOP (Normal :
10-21 mmHg)

78. Aimed to reduce IOP.
Medications
Surgery:
Iridectomy for Acute
Glaucoma Treatment
Trabeculoplasty
Chronic Glaucoma –
Medications and
eyedrops
Concern: Safety

79.  Medical follow-up and eye medication
will be required for the rest of your life.
 Eyedrops must be continued as long as
prescribed, even the absence of
symptoms
 Avoid driving 1-2 hours after the
administration of miotics
 Prevent complications
 Bright lights and darkness are not
harmful
 There is no apparent relationship
between the vascular hypertension and
ocular hypertension.
 Report any reappearance of symptoms
 Avoid the use of mydriatric or cyclopegic
drugs. (atropine)

80. Clouding of the normally
clear and transparent lens
of the eyes.
Cause by Oxidative damage
to lens proteins that occurs
with aging.
 Other causes:
 Heredity
 diabetes
 poor nutrition
 hypertension
 excessive exposure to sunlight
 cigarette smoking
 high alcohol intake
 Eye trauma.

81. Senile Cataract –
due to normal
aging process as
early as 40
Traumatic Cataract Types of
– hard Cataract
blow, puncture, cut
or burn.
Secondary

82. With gradual loss of vision
(blurred, misty or dimmed)
Complaints of being fuzzy,
sensitive to glare and halo-effect
around lights.
No pain or discomfort
Decrease night vision
Yellowing of the lens.
trouble distinguishing colors
Pupil changed into cloudy white.
Decreased visual acuity.
Recurrent eyeglass prescription
changes.

83. Improved
visual
acuity, depth
perception.
Complications: Surgery
retinal
detachment, in
fection and
macular
edema.

84. Avoid rubbing or
pressing on the eye.
Avoid bending at the
waist or lifting heavy
objects for at least 1 ACTIVITIES
month NOT TO DO
Avoid straining with AFTER A
bowel movements CATARACT
Avoid taking showers SURGERY
and shampooing hair
for specified time as
instructed.
Limit reading.

85. Sleep on back
or unaffected
side.
Apply metal
eye shield at
night.
Wear glasses
indoors
Proper
handwashing

86. Most common
cause of blindness
for those over age
60.
Damage or
breakdown of the
macula and
subsequent loss of
central vision due
to Macular
Degeneration.

87. Dry (Nonexudative) –
involutional macular
degeneration.
Breaking down or thinning
of macular tissue related to
the aging process. Types:
Gradual vision loss.
Wet (exudative) – rapid and
severe vision loss.
Abnormal blood vessels
form and hemorrhage.

88. Difficulty performing
tasks (reading and
sewing)
Decreased central
vision
Seeing images are Signs and
distorted Symptoms:
Decreased color vision
(colors look dim)
Central Scotoma
(sometimes)

89. Photodynamic
Therapy – a special
laser to seal leaking
blood vessels.
Retinal Cell
Transplantation
Medications: Treatment
Ranibizumab
(Lucentis)
Bevacizumaba
Pegaptanib

91. Auricle – becomes
elongated, with a wrinkled
appearance.
Auditory canals – narrows
Hairs lining the canal becomes
coarser and stiffer.
Cerumen glands atrophy
Tympanic membrane –
dull, retracted and gray
appearance.
Degeneration of the ossicular
joints in the middle ear
Decreased vestibular
sensitivity.

92. Age related
balance decline
Decreased sensory
input, slowing of
motor responses
and
musculoskeletal
limitations.

93. Reversible, overlooked
cause of conductive
hearing loss.
Cause: physiologic
changes with aging –
atrophic changes in the Cerumen
sebaceous and apocrine Impaction
glands.
Impaired communication
– social isolation and
depression.

94. Hearing
loss, feeling of
fullness in the
ear, itching and
tinnitus.
Intervention
Read the
protocol for
cerumen
removal page
740

95. Is the annoying
combination of both
conductive and
sensorineural hearing loss.
Subjective sensation in the
ear, defined as the
ringing, buzzing or hissing.
Cause:
noise, toxins, cochlear
nerve and age related
changes in the organs of
hearing.

96. Subjective
Objective –
rare
Unilateral –
associated with
more serious
diseases
(Meniere’s
disease)

97. Treat the correctable
problems.
Softening loud sounds
through improved
acoustic
Use a protective ear
plugs
Avoid ototoxic
substances
(foods, drugs)

98. sensorineural hearing loss
The most common form
of hearing loss in older
adult.
Bilateral, difficulty hearing
high pitched tones and
conversational speech.

99. Increasing volume on
television or radio.
Tilting head toward the
person speaking
Cupping hand around the
ear.
Watching the speaker’s
lips
Speaking loudly
Not responding when
spoken to

100. Focus on aural
rehabilitation
and facilitation of
communication.
Aural
rehabilitation
Auditory training
speech and reading
training
hearing aids.

101. should not be considered as
a normal part of aging.
Benign paroxysmal positional
vertigo (BPPV) – severe
episodes of vertigo
precipitated by a particular
change in head position.
Ampullary dysequilibrium –
vertigo or disequilibrium
associated with rotational
head movements.

102. Macular disequilibrium – vertigo
precipitated by a change of head position
in relation to the direction of gravitational
force.
Vesicular ataxia of aging – constant feeling
of imbalance with ambulation.
Meniere’s disease – an uncommon disease
seen most often in older
women, characterized with severe vertigo
accompanied and usually preceded by
tinnitus and progressive low frequency
sensorineural hearing loss.

103. Pharmacological
treatment
Anti-vertiginous drugs
Meclizine (antivert)
Diphenhydramine
(Benadryl)
May cause
drowsiness, avoid alcoholic
beverages
Diuretic
Hydrochlorothiazide
(Hydrodiuril)
Remove the excess
endolymph fluid

104. No complete cure
Measures to reduce
dizziness
Move slowly
Avoid bright glaring
Nursing
lights (quiet darkened interventions
room is preferred) For Vertigo
If vertigo occurs
during ambulation lie
down immediately
and hold the head
still.