NCM116 PERCEPTION AND COORDINATION

ALZHEIMER’S DISEASE (AD)

- Chronic brain disease that is type of dementia (most common form of dementia
(Dementia is not a type of disease but is rather a general term for the impaired ability to
remember, think, or make decisions that interferes with doing everyday activities)
- Progressive disease beginning with mild memory loss and possibly leading to loss of the
ability to carry on a conversation and respond to the environment.
- Women are more likely to develop the disease (women tend to live longer)
- Neurons are tend to die
- No cure

ETIOLOGY and PATHOPHYSIOLOGY

- Cause unknown (genetics, age-related changes in the brain, environment and lifestyle
factors)

NOTE: there are billions of neurons in the brain and these neurons are very busy all the
time. They constantly communicating with each other, sending signals and releasing
neurotransmitters to help communicate their messages
How a message is sent?
Dendrites are waiting for an electrical signal, and take it to the cell body of neurons. The
cell body will process the message that it receives. Synapse release neurotransmitters
(acetylcholine and glutamate). Axons carried the message away from the cell body. The
neurotransmitter will send the message to musles, glands or whatever they are targeting
with the message.

Microglia – hang out around the neuron, survey around the neuron environment and if
they see any debris or chemical they eat it.

- Development of plaques (beta-amyloid protein)

Plaques form outside the neuron

Cause impede communication of neuron to neuron and other structures

Development of neurofibrillary tangles (protein called TAU)

Form within the neuron itself

Brain tissue can shrink (brain atrophy)

Progressive loss of memory (AD)

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Parts of brain affected

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Hippocampus- (middle deep part of brain) learning

new things and memory
*navigating around of finding objects you place somewhere
Enterhinal area – understanding time, memory, sense of direction
Amygdala – emotional memory
*how you respond to environment
Early AD
Loss of memory start suddenly and gradually, progressively get worst where the patient will no
longer have memory.

If plaques and tangles continue to form, it will affect the cerebral cortex that surrounds the
cerebrum
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SIGNS and SYMPTOMS

Apraxia – can’t perform certain motor movement
Example: Brushing teeth
Aphasia – can’t understand speech or create it
Example: giving them instruction they can’t understand it.
*Use card or image of what they needed to do.
Agnosia – can’t recognized objects, people or interpret they senses
Example: urinate – they do not know how to do it (senses)
Spoon they do not know what is the use, food to eat ( they do not know what their eating)
Amnesia – memory loss
Anomia – can’t recall name of objects

Stages of Alzheimer’s disease

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Diagnostics
Cognitive assessment – ask patient to test memory, judgement and thinking
Mental Evaluation
MRI & CT Scan – to make sure no tumors or stroke has occurred
Amyloid PET scan – look for beta-amyloid markers is the brain
Biomarkers
Spinal Tap – remove CSF and test it for the proteins

Nursing Interventions
1. Helping the patient identify sign & symptoms of AD
2. Medication
3. Educating how the disease progresses
7M’s
1. Memory – reorient, remind, remain patient, keep simple, do not scold the patient (it may
cause them agitated)
*use imagery
*give simple activity like foldng clothes

2. Movement – independent as allowed, routines, exercise, fun games

*memory games

3. Mental Health – calm, distract, and do not hurry them, hallucinations

*well-lit room, remove reflective items
*sundowners – more confuse during evening
Decrease sundowning: low nois, clam, relaxing environment
No caffeine at night
Routines are important
Exercise and rest
Avoid long late naps

4. Maintain safety – beware of driving, hide keys

Supervise cooking
Beware of wandering
S&Sx of Wandering
- get lost or forget places
- taking longer than normal to return from a place
- having trouble finding rooms in the house
- talking about going somewhere or visiting someone
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Promote safety during wandering period

Wear ID bracelet or gps (watch)
Avoid stressful, unfamiliar places (crowds)
Needs met (bathroom, food, drinks)
Display sign providing cues (labels, warnings)
Exercise is important (activity they enjoy)
Remove access to doors/windows (locks, alarms)

5. Maximise communications
Pick one question/instruction at a time (repeat)
*asked closed ended question
Avoid correcting or arguing (watch tones/expressions to avoid)
Take time for patient to speak/respond
Identify yourself from front, not side or back (it may scare them)
Eye contact on eye level, not from above (intimidation)
Nonverbal communication helpful (act, point, use image)
Talk in slow, normal, clear tone; eliminate noise (patient can hear and understand you)

6. Medical Needs- hygiene (bathing, grooming, mouth care, dressing)

*hydration – thirst, loss of interpretation of thirst)
*Nourishment – loss the sensation of taste, trouble swallowing (dysphagia)
Intervention for eating food:
- Don’t overwhelm with options
- Offer healthy foods patient likes to eat
- Use finger foods that are soft and easy to chew
- Help patient focus on meal rather than the environment; eat with them

7. Medications
Cholinesterase Inhibitors – Cholinesterase are enzyme helps breakdown acetylcholine
Donepezil
Rivastigmine
Galantamine
Acetylcholine – low in Alzheimer’s disease (enzyme that helps in thinking and memory)
Side Effects : GI upsets (NVD) (administer with food to reduce side effects)
Muscle spasm
Bradycardia (risk for falls) measure heart rate
NMDA antagonist – memantine – effect the neurotransmitter glutamate which works with
NMDA receptor cause calcium to go in the neuron and fire it up. Excess: damage neuron
Glutamate – excitatory neurotransmitter
Aducanymab – given via IV q 4 weeks, decrease beta-amyloid plaques
Side effect: brain bleeding or swelling
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HUNTINGTON’S DISEASE (HD)

- An inherited disorder that causes nerve cells (neurons) in parts of the brain to gradually
break down and die. The disease attacks areas of the brain that help to control voluntary
(intentional) movement, as well as other areas.
- The degeneration is pronounced on the striatum (caudate and putamen) early but later
it affects other parts of the brain.
- 50% chance that an affected parent will pass the disease to an offspring
- 10% of cases can result from spontaneous mutation
- Common at the age of 30s and 40s but can occur earlier
- It results from “trinucleotide repeat expansion” (Cytosine-Adenine-Guanine) of the gene
codes for the protein huntingtin on chromosome 4.
o This results in polyglutamine expansion, (CAG) codes for glutamine. The length of
the repeat the severity of the disease
o Normal glutamine residue: 6-35
- No cure
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ETIOLOGY/PATHOPHYSIOLOGY
- Cause by a mutation in the gene for a protein called huntingtin
o The HTT gene provides instructions for making a protein called huntingtin. Although the exact
function of this protein is unknown, it appears to play an important role in nerve cells (neurons) in
the brain and is essential for normal development before birth
o Everyone has the huntingtin gene, but only those that inherit the mistake, known as the HD
mutation, will develop HD and risk passing it on to their children.

Inherited as autosomal dominant pattern:

For example
Gene: Father: Aa
Mother: AA
*capital A is normal, small a is abnormal gene, when you inherit both the capital A from parent, it is
normal, you cannot have the disease but if you inherit the small a from father and capital A from mother
you can get the disease.
There is destruction of cells in the caudate nucleus and putamen areas of the basal ganglia and
extrapyramidal motor system. The neurotransmitters, gamma-aminobutyric acid (GABA) and
Ach are decreased. Dopamine is not affected, but the decrease of Ach cause relative increase of
dopamine in the basal ganglia. The excess dopamine causes uncontrolled movement in
Huntington’s chorea.
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CLINICAL MANIFESTATIONS
- Motor changes
o Chorea – brief, irregular, involuntary, movement that appears to flow from one
muscle to another
 uncontrollable dance-like movements
For some people, chorea can make it harder to walk, which increases the chances of
falling.
o Athetosis – slow involuntary writing or twisting movement of the hands, finger
and toes.
 Unusual eye movements - The eye movements can happen early in
the disease.
o Rigidity
Some people with HD do not develop chorea; instead, they may become rigid (stiff) and
move very little or not at all. This condition is called akinesia. Other people may start out with
chorea but become rigid as the disease progresses. Some individual have unusual fixed
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(unchanging) postures, which is known as

dystonia. The two movement disorders (akinesia and dystonia) can blend or alternate.
o Slurred speech and problems with swallowing, eating, speaking, and especially
walking
- cognitive changes
o Problems with attention or judgment
o Prioritizing (deciding which things are more important to do and which are less
important)
o Trouble with driving,
o Difficulty organizing, learning new things, remembering a fact, putting thoughts
into words, or answering a question.
o Difficulty solving problems or making decisions.
These cognitive changes get worse as the disease progresses, until people with HD are not able
to work, drive, or care for themselves.
- Changes in behaviour
o mood swings
o feeling irritable (cranky)
o not being active
o feeling apathetic (uninterested)
o Depressed
o Angry.
These symptoms may decrease as the disease progresses. But in some people, the symptoms
can continue and may include angry outbursts, thoughts of suicide, deep depression, and
psychosis (losing touch with reality). People with HD may withdrawal from social activities.

DIAGNOSIS
The diagnosis is purely medical. It can be confirmed by genetic testing.
 Neurological exam and medical history—A neurologist will conduct an in-depth
interview to obtain the medical history (including any family history, called a pedigree or
genealogy) to rule out other conditions. Neurological and physical exams may review
reflexes, balance, movement, muscle tone, hearing, walking, and mental status.
 Diagnostic imaging—In some cases, especially if a person's family history and genetic
testing are inconclusive, the physician may recommend brain imaging, such as computed
tomography (CT) or, more likely, magnetic resonance imaging (MRI). As the disease
progresses, these scans typically reveal shrinkage in parts of the brain and enlargement
of fluid-filled cavities within the brain called ventricles. 
 Genetic tests—Genetic testing can confirm or rule out a suspected genetic condition or
help determine a person's chance of developing or passing on a genetic disorder.
o The most effective and accurate method of testing for HD—called the direct
genetic test—counts the number of CAG repeats in the HD gene, using DNA
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taken from a blood sample. The

presence of 36 or more repeats supports a diagnosis of HD. A test result of 26 or
fewer repeats rules out HD.
o An older genetic test, called linkage testing (also called prenatal exclusion
testing) requires a sample of DNA from a closely related affected relative,
preferably a parent, to identify markers close to the HD gene and to determine if
a fetus has inherited a chromosome 4 mutation from an affected grandparent. A
version of the linkage method is sometimes used for prenatal testing.
o Prenatal testing is an option for people who have a family history of HD and are
concerned about passing the disease to a child. Prenatal testing can be done
using either the direct method or the linkage method.

MEDICAL MANAGEMENT

1. Although no treatments halts or reverse the underlying processes, several medications

prescribed.
2. Disease management includes rehabilitative therapy, teaching, counseling and professional
legal, financial and estate planning advice.
3. Pharmacological methods of treatment are carefully considered when treating
Huntington’s disease. Many medications can be used and it is important to assess the
combination of medications that are used.
4. Medications administered to manage Huntington’s disease:
 Rilutek (riluzole) is currently being studied to decrease cognitive manifestations
 Skeletal muscle relaxants to modify the choreiform movements
 Antipsychotics to block the dopamine receptors in the brain
 Antidepressants to help control the chorea, behavioral changes and depression

Side effects of drugs used to treat the symptoms of HD may include fatigue, sedation, decreased
concentration, restlessness, or hyperexcitability. These drugs should be only used when HD
symptoms create problems for the person living with HD.

NURSING DIAGNOSIS

 Risk for injury from falls and possible skin breakdown (pressure ulcers, abrasions), resulting
from constant movement
 Imbalanced nutrition: less than body requirements due to inadequate intake and
dehydration resulting from swallowing or chewing disorders
 Risk for aspiration related to swallowing difficulty
 Anxiety and impaired communication from excessive grimacing and unintelligible speech
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 Disturbed thought processes and impaired

social interaction

NURSING MANAGEMENT

1. Prevent injury and possible skin breakdown

 Pad the sides and head of the bed
 Keep the skin meticulously clean
 Encourage ambulation with assistance to maintain muscle tone
 Secure the patient in bed or chair with padded protective devices making sure they
are loosened frequently
2. Keep patient as close to upright as possible while feeding. Stabilize patient’s head gently
with one hand while feeding
3. The nurse needs to educate and support the patient and family as they adjust to the
lifestyle changes that are required.
4. The actions and potential side effects of medication regimen need to be taught, monitored
and adjusted to the desired patient response.
5. Regular moderate exercise can reduce stiffness and tremors.
6. As the disease progresses, the patient and family will require more assistance with
activities of daily living, emotional support, and potential financial concerns.

MULTIPLE SCLEROSIS (MS)

- Auto immune disease that affect the myelin sheath of neurons in the central nervous
system (Brain & Spinal cord)
- Women are more frequently affected than males ages of 20 to 40 years.
- Genes encoding for (HLA-DR2)-identify and bind foreign molecules
- Environmental factors: infections and vitamin D deficiency
Myelin is a substance produce by oligodendrocytes and makes up the protective sheath (myelin
sheath) that coats nerve fibers (axons).

ETIOLOGY/PATHOPHYSIOLOGY
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Demyelination happens when immune system

inappropriately attacks and destroys the myelin. It makes the communication between neurons
break down, ultimately leading to all sorts of sensory, motor and cognitive problems. It slows
down or blocks messages from the brain to the bod the brain to the body. When the
inflammation goes away, it leaves behind scarring of the myelin sheath (sclerosis). If the attacks
are frequent, they can lead to permanent damage to the underlying nerves.

Mechanism by which immune cells participate in the pathogenesis of multiple sclerosis.T cells recognize
myelin epitopes and activate macrophages to damage myelin by phagocytosis. Cytokines and toxic
mediators such as NO released by T cells, microglia, and macrophages cause myelin damage.
Furthermore, autoantibodies through binding to myelin and activating complement facilitate
phagocytosis mediated by macrophages.

TYPES OF MULTIPLE SCLEROSIS

1. Relapsing-remitting MS—(most common) Symptoms in this type come in the form of
attacks. In between attacks, people recover or return to their usual level of disability.
When symptoms occur in this form of MS, it is called an attack, a relapse, or
exacerbation. The periods of disease inactivity between MS attacks are referred to as
remission. Weeks, months, or even years may pass before another attack occurs,
followed again by a period of inactivity. Most people with MS are initially diagnosed
with this form of the disease.
2. Secondary-progressive MS—People with this form of MS usually have had a previous
history of MS attacks but then start to develop gradual and steady symptoms and
deterioration in their function over time. Most individuals with severe relapsing-
remitting MS may go on to develop secondary progressive MS if they are untreated.
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3. Primary-progressive MS—this type of MS

is less common and is characterized by progressively worsening symptoms from the
beginning with no noticeable relapses or exacerbations of the disease, although there
may be temporary or minor relief from symptoms.
4. Progressive-relapsing MS—the rarest form of MS is characterized by a steady worsening
of symptoms from the beginning with acute relapses that can occur over time during the
disease course.

SIGNS AND SYMPTOMS

Dysarthria – difficult or unclear speech caused by plaques in the brainstem
- Interfere with:
 conscious movement (eating & talking)
 unconscious movement (swallowing)
Nystagmus – involuntary eye movements caused by plaques in nerves of eyes
- optic nerve (loss of vision, optic neuritis)
- movements (pain, double-vision)
Intention tremors – caused by plaques along the motor pathway in the spinal cord which can
affect outbound signals like skeletal muscle control.
- Muscle weakness and muscle spasms
- Tremors and ataxia (loss of balance and coordination)
- In serious cases may lead to paralysis
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Plaques in the sensory pathways can affect

inbound signals-like sensations from skin
- Numbness
- Pins and needles
- Paresthesias which often a tingling feeling but it may be a painful itching or burning
sensation
+Romberg’s sign – lesions in the cerebellum area
Lhermitte’s sign – when an electric shock runs down the back and radiates to the limbs
when a person bend their neck forward.
Plaques in autonomic nervous system (bowel and bladder dysfunction)
- Constipation and Urinary incontinence
Uhtoff’s sign – heat makes the S&Sx worst.
Higher order activities of brain
- Poor concentration and critical thinking
- Deppresion and anxiety

DIAGNOSIS
MRI - shows multiple nervous system lesion (white matter plaques) since this region tends to
have a lot of myelin
CSF - there might be a lot of antibodies, which indicates an auto immune process
VISUAL EVOKED POTENTIAL – measures the nervous system’s response to stimuli

TREATMENT (no cure)

 Beta-interferon (AVONEX) – decreases the number of relapse of symptoms by decreasing
the inflammation and the immune system response.
SE: risk for infection because it decreases WBC
 Corticosteroids agents, such as Prednisone (Orasone); methylprednisolone or (Solu-
Medrol); dexamethasone (Decadron) maybe used to help decrease symptoms and induce
remissions through anti-inflammatory effects.

 Immunomodulatory agents, such as Interferon, cyclosporine, azathioprine, methotrexate

maybe used to help decrease symptoms and induce remissions; treatment includes
combination therapy using two or more of these agents.
 Other Drugs: Antianxiety agents, such as chlordiazepoxide hydrochloride (Librium), may be
prescribed to manage mood swings; baclofen (Lioresal) or dantrolene (Dantrium) may be
used to relieve muscle spasticity; and patients with urinary symptoms may require
behanechol (Urecholine) or oxybutynin (Ditropan).
 For bladder issues:
 Oxybutynin - anticholinergic that helps the over active bladder by relaxingthe
bladder muscle to prevent contractions
 Betanechol – cholinergic that helps with the emptying the bladder by helping
with bladder contractions
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NURSING DIAGNOSIS
 Impaired physical mobility related to fatigue and weakness.
 Risk for injury
 Impaired urinary elimination
 Risk for ineffective coping

NURSING INTERVENTION

1. Provide bed rest during exacerbation.

2. Protect the client from injury by providing safety measures.
3. Place an eye patch on the eye for diplopia.
4. Monitor for potential complications such as urinary tract infections, calculuses, decubitus
ulcers, respiratory tract infections, and contractures.
5. Promote regular elimination by bladder and bowel training.
6. Encourage independence.
7. Assist the client to establish a regular exercise and rest program.
8. Instruct the client to balance moderate activity with rest periods.
9. Assess the need for and provide assistive devices.
10. Initiate physical and speech therapy.
11. Instruct the client to avoid fatigue, stress, infection, overheating, and chilling.
12. Instruct the client to increase fluid intake and eat a balanced diet, including low-fat, high-
fiber foods and foods high in potassium.
13. Instruct the client in safety measures related to sensory loss, such as regulating the
temperature of bath water and avoiding heating pads.
14. Instruct the client in safety measures related to motor loss, such as avoiding the use of
scatter rugs and using assistive devices.
15. Instruct the client in the self-administration of prescribed medications.
16. Provide information about the National Multiple Sclerosis Society.