Management of

Patients with Cerebral

Infections
Meningitis

● Inflammation of the meninges, which cover and protect the

brain and spinal cord.

● THREE MAJOR CAUSES: bacteria, virus, fungi

● Classified as:

- septic- caused by bacteria (Streptococcus

pneumoniae, Neisseria Meningitidis)

- Aseptic- caused by virus/ secondary to cancer/weak immune

system
Pathophysiology

● Infection generally originate in two ways:

- Bloodstream as a consequence of other infection

- Direct spread after a traumatic injury of facial bones or

secondary to invasive procedures.

● Once the organism enters the bloodstream, it crosses the

blood-brain barrier and proliferate in the CSF.

● The host response is inflammation of the subarachnoid and

pia mater. ● Then, increased ICP because of little space for
expansion of the cranial vault.
● CSF circulates through the subarachnoid space, where
inflammatory cellular materials from affected meningeal
tissue enter and accumulate.

Clinical Manifestations

● Headache and fever are frequently the initial symptoms

that remains high throughout the course of illness.

● Headache is steady or throbbing and severe as a

result of meningeal irritation.

● Meningeal irritation results in a number of well recognized

signs common to all type of meningitis.
 - Neck immobility- a stiff and painful neck (nuchal rigidity)

- Kernig’s sign- when patient is in lying position with the thigh

flexed on the abdomen, the leg cannot be completely
extended. Bilateral Kernig’s sign suggests meningeal
irritation.
Clinical Manifestations

- Positive Brudzinski’s sign- when the patient’s neck is flexed ,

flexion of the knees and hip is produced, when the lower
extremity of one side is passively flexed, a similar
movement is seen on the other side.

- Photophobia- sensitivity to light

- A rash can be a striking feature of N. meningitidis

infection, occurring in about half of patients with
this type of meningitis.

Clinical Manifestations
OTHER MANIFESTATIONS:

● Skin lesion ranging from petechial rash with purpuric lesions to

large areas of ecchymosis in 50% of patients.

● Disorientation and memory impairment are common in the

early course of the disease.

● Lethargy, unresponsiveness, and coma as

the illness progresses. ● Seizure
● Increased ICP, herniation, brain stem compression
Assessment and Diagnosis

● CT, MRI

● Lumbar puncture- to assess the CSF (cloudy/clear),

check the presence of blood, increased WBC

- Neurologic signs: ALOC, papilledema, neurologic

deficits, new onset of seizure,
immunocompromised state.

● Prevention- infection control

- Meningococcal conjugated vaccine given to 11-12 years of age,

booster at 16.

- Close contact with patient: antimicrobial prophylaxis

[rifampin(Rifadin), ciprofloxacin (Cipro), ceftriaxone
(Rocephin)]
 - Prophylaxis should be started 23 hours after

- Vaccination with pneumonia

Medical Management

● Administration of antibiotic that crosses the blood-brain

barrier into the subarachnoid space to halt the
multiplication of bacteria.

- Penicillin G in combination with one of the

cephalosporins (ceftriaxone sodium, cefotaxime
sodium) intravenously

- Dexamethasone (Decadron) often use as

adjunct in bacterial and pneumococcal
meningitis.

● IVF for shock and dehydration.

Nursing Management

● Instituting infection control precautions until 24 hours

after initiation of antibiotic therapy (oral and nasal
discharge is considered infectious)

● Assisting with pain management due to overall body

aches and neck pain ● Assisting with getting rest in a
quiet, darkened room
● Implementing interventions to treat the elevated
temperature, such as antipyretic agents and
cooling blankets

● Encouraging the patient to stay hydrated either

orally or peripherally ● Ensuring close neurologic
monitoring
Nursing Management

● Protecting the patient from injury secondary to seizure activity or

altered LOC

● Monitoring daily body weight; serum electrolytes; and urine

volume, specific gravity, and osmolality, especially if
syndrome of inappropriate antidiuretic hormone (SIADH)
is suspected

● Preventing complications associated with immobility, such as

pressure ulcers and pneumonia
Brain Abscess

● Collection of infectious material within

the tissue of the brain. ● Bacteria are the
most common causative organisms.
● Rare in people who are immunocompetent, may occur in
 people with otitis media, rhinosinusitis.

● 50% of brain abscess is otogenic in origin (e.g. mastoiditis).

● May also result from intracranial surgery, penetrating

head injury, tongue piercing.

● Organisms causing brain abscess may reach the brain by

hematologic spread from the lungs, gums, tongue/heart or
from a wound or intraabdominal infection.
Clinical Manifestations

● Result from alterations in intracranial dynamic such as edema,

brain shift, or infection of the location of abscess.

● Headache that is worse in the

morning is the most prevalent. ● Fever
may or may not be present.
● Vomiting and focal neurologic deficits, such as
weakness and decreasing vision that reflects the
area of the brain involved.

● As the abscess expands: symptoms of increased ICP, such

as decreasing LOC and seizures.
Clinical Manifestations

● Frontal Lobe: Hemiparesis, expressive aphasia, seizure, frontal

headache.

● Temporal Lobe: localized headache, changes in

vision, facial weakness, receptive aphasia.

● Cerebella abscess: occipital headache, ataxia, nystagmus.

Diagnosis:

● CT Scan

● Aspiration of abscess guided by CT scan

or MRI for blood culture. ● EEG
Management

Medical Management

● Controlling increased ICP

● Draining the abscess

● Antimicrobial therapy based on the

results of C and S. ● Ceftriaxone is usually
started then adjusted with the results of C
and S. Nursing Management
● Continue assessing the neurologic status.
● Administer prescribe medication.

● Assessing the response to treatment.

● Providing supportive care.

Herpes Simplex Encephalitis

● Is an acute inflammatory process of the brain tissue.

● Herpes Simplex Virus (HSV) is the most common cause of

acute encephalitis in the US.

➢ Herpes Simplex Virus Encephalitis

➢ Arthropod- Borne Virus Encephalitis

➢ Fungal- Encephalitis

➢ Creutzfeldt-Jacob Disease
Pathophysiology

● Encephalitis involves local necrotizing hemorrhage

that becomes more generalized.

● Edema follows necrotizing hemorrhage.

● Then progressive deterioration of nerve cell bodies.

Encephalitis

HSV Encephalitis

● Initial Manifestations: Fever, headache, confusion, hallucination

● Focal Neurologic symptoms: fever, headache,

behavioral changes, focal seizures, dysphasia,
hemiparesis, and altered LOC.
HSV Encephalitis

Diagnostic Findings:

● MRI is the neuroimaging of choice for early detection of changes.

● EEG shows slowing or focal changes in the temporal

lobe in majority of patients.

● Lumbar puncture has high opening pressure with normal

glucose and high protein in CSF.

● Viral culture almost always negative.

● Polymerase chain reaction (PCR), it identifies DNA

bands of HSV-1 in CSF especially on the 3rd to 10th
day.
 Medical Management

● Antiviral agents

- Acyclovir (Zovirax)

- Ganciclover (Cytorene)

- Treatment is up to 3 weeks, slow IV

over an hour. - Early administration is
well tolerated and improves prognosis.
Nursing Management

● Assessment of neurologic functions.

● Comfort measures to reduce headache.

- Dimming the light, limiting noise and visitors,

grouping of nursing interventions,
administering analgesic, opioid analgesic.

- May mask neurologic symptoms.

Encephalitis

HSV-1 Encephalitis

● Cause: necrotizing hemorrhage that becomes generalized,

followed by edema. ● S/SX: fever, headache, confusion,
hallucination, hemiparesis, ALOC, dysphasia ● Assessment:
EEG, CSF examination to diagnose.
● Management: Antiviral: Zovirax (Acyclovir)- choice

- Assess neurologic status

- Comfort measures to reduce headache, limiting

noise, visitors, lights - Promote safety- ALOC
- Monitor blood chemistry.
Arthropod-Borne Virus
Encephalitis● Transmitted by blood
feeding arthropods like mosquitoes/ticks ●
5 main arboviral encephalitis
- Eastern equine encephalitis

- Western equine encephalitis

- St. Louis encephalitis

- La Crosse encephalitis

- West Nile Virus

Arthropod-Borne Virus Encephalitis
 Pathophysiology:

● Viral replication occurs at the site of mosquito bites.

● The immune response attempts to

control viral replication. ● If immune
response is inadequate viremia
results.
● Virus gains access to the CNS via the olfactory tract resulting in
encephalitis.

● It spreads from neuron to neuron gray matter, the

brainstem and the thalamus.

● Meningeal exudates aggravate the clinical

presentation by meningeal irritation then
increasing ICP.

● St. Louis and West Encephalitis- commonly affect adults

Arthropod-Borne Virus Encephalitis

Clinical Manifestations:

● Occur along a continuum.

● Some cases have flu-like symptoms such

as headache and fever. ● Unique to St.
Louis is SIADH and hyponatremia.
● Incubation period of St. Louis is 4 to 12 days with abrupt
onset of symptoms. - fever, headache, nausea, dizziness,
malaise.
- CNS: stiff neck, confusion, dizziness, and tremors.

- Coma can occur in severe cases,

mortality increases with age. - Seizures
are indicator of poor prognosis, common
to St. Louis.
Arthropod-Borne Virus Encephalitis

Diagnostic Findings:

● Clinical presentation and location and dates of recent travel

because certain viruses are endemic in some
geographical areas.

● MRI demonstrate inflammation of the:

- Basal ganglia in St. Louis

- Periventricular area in West Nile.

● IgM antibodies in West Nile virus.

 ● EEG can identify abnormal brain waves.
Arthropod-Borne Virus Encephalitis

Medical Management:

● No specific medication, symptomatic management is the key,

like controlling seizures and increased ICP.

● Interferon is useful in St. Louis but no

specific drug is indicated. Nursing
Management:
● Carefully assess neurologic status and
identifies improvement or deterioration
of patient’s condition.

● Public education addressing the prevention of arboviral

encephalitis.
Encephalitis

Arthropod-Borne Virus Encephalitis

● Cause: mosquitoes, ticks, mosquito bite- virus

gains access to CNS via olfactory tract, affect
gray matter, brain stem, thalamus.

● S/SX: Flu-like symptoms (headache+fever)

● St. Louis encephalitis, La Crosse encephalitis, West Nile

Virus Encephalitis (Arthropod vectors)

● Management: Control seizure, and Increased ICP management

Fungal Encephalitis● Fungal infection - Fungal spores enter the body via
of the CNS ● Example of Fungi: inhalation
- Cryptococcus neoformans -
Blastomyces dermatitidis - - Initially infect the lungs, causing
Histoplasma capsulatum - Aspergillus vague respiratory symptoms.
fumigatus - Candida
- The fungi may enter the
- Coccidioides immitis
bloodstream causing fungemia.

- When fungemia overwhelms the

immune response, fungus may
● Pathophysiology: spread to CNS and cause meningitis,
encephalitis, brain abscess
Clinical Manifestations:

● Fever, malaise, headache, meningeal signs

● Change of LOC, or cranial nerve dysfunction

● Increased ICP r/t hydrocephalus

● C. neoformans associated with skin lesions.

 ● H. capsulatum is associated with seizures.

● Aspergillus fumigatus may cause ischemic or hemorrhagic stroke.

Fungal Encephalitis

Diagnostic Findings:

● History of immunosuppression like HIV

● History of travels

● CSF: elevated WBC and protein levels, decreased glucose

● Candida may be cultured.

Medical Management:

● Antifungal Medications: fluconazole (Diflucan), flucytosine

(Ancobon)

● Amphotericin B is used for progressive fungal infection that

does not improve with conventional therapy.
Fungal Encephalitis

Nursing Management:

● Monitor ICP

● Administer diphenhydramine and paracetamol 30

minutes before giving Amphotericin B to prevent
flulike side effects.
Creutzfeldt-Jakob and Variant Creutzfeldt-Jakob Disease

● Belong to a group of degenerative infectious neurologic

disorders called “transmissible spongiform
encephalopathies (TSE)”.

● CJD is very rare and no identifiable cause.

● vCJD, the human variation of bovine spongiform

encephalopathy, commonly known as mad cow disease.

● TSE is caused by prions.

● Prions are particles smaller than the virus that are

resistant to standard methods of sterilization.

● CJD and vCJD lack CNS stimulation.

● The incubation period of vCJD shorter (less than 10 years).

Creutzfeldt-Jakob and Variant Creutzfeldt-Jakob
DiseasePathophysiology:
● The prions cross the blood-brain barrier.
 ● Deposited in the brain tissue and causes degeneration of the brain
tissue.

● Cell death occurs and spongiform changes (spongy vacuole)

are produced in the brain surrounded by amyloid plaque.

Clinical Manifestation:

● Psychiatric symptoms: early in vCJD, late in CJD

● The mean age at onset: vCJD is 27, CJD is 65.

Creutzfeldt-Jakob and Variant Creutzfeldt-Jakob
DiseasevCJD:
● Affective symptoms, like behavioral changes

● Sensory disturbance

● Muscle spasm and rigidity

● Dysarthria, incoordination

● Cognitive impairment, sleep disturbance

Creutzfeldt-Jakob and Variant Creutzfeldt-Jakob
DiseaseCJD:
● Memory loss

● Involuntary movement

● Paralysis

● Mutism as the disease progresses

● vCJD survive an average of 22 months.

● CJD less than one year.

Creutzfeldt-Jakob and Variant Creutzfeldt-Jakob
DiseaseDiagnostic Findings:
● CSF presence of kinase inhibitor which indicates
neuronal death but not specific of the disease.

● EEG reveals a characteristic pattern over the

duration of the disease. ● MRI
Medical Management:

● No effective treatment.

● Symptomatic and palliative.

Management of Patients
With Degenerative
Neurologic Disorders

Degenerative Neurologic Disorders

● These disorders cause progressive decline

in neurologic function ● Some progress
quickly, over months to 1-2 years ● Some
progress more gradually, sometimes over
decades.
Alzheimer’s Disease
Alzheimer's Disease (AD) and related Dementias

● Dementia- refers to the loss of memory, reasoning,

judgment and language skills

● Cognition- the act or process of thinking,

perceiving and learning ● Cognitive activities
that are impaired
➢ decision making, judgment, memory

➢ spatial orientation, thinking, reasoning, calculation

➢ personality and behavioral changes, verbal communication

Alzheimer's Disease

● is a progressive, irreversible, degenerative neurologic disease that begins

insidiously and is characterized by gradual losses of cognitive functions and
disturbances in behavior and affect.

● Alzheimer's disease, the most common form of dementia among people

over age 65. Affects about 5 million Americans.

● Prevalence of AD doubles every five years after the age of 65 ● Estimates

indicate that nearly half of people older than 85 have AD ● Brain quickly
injured from hypoxia, reduced blood flow or drugs
Alzheimer's Disease

● MULTI-INFARCT (multiple strokes), is the second

most common cause of irreversible dementia

● Blood clots block small vessels in the brain and

destroy brain tissue ● Typically occurs in men
above 50
● Overtime leads to progressive decline in cognition
Pathophysiology

● AD disrupts the three neuronal processes that

keeps neurons healthy: communication,
metabolism and repair
 ● Alois Alzheimer termed these changes as beta
amyloid plaques and neurofibrillary tangles

● Neurons supported by microtubules, stabilized by protein tau

Pathophysiology

● In AD, tau changed chemically and becomes

tangled, once tangled, the tubules degenerate
and the cells they support

● These destruction leads to memory failure, personality changes

and problems carrying ADLs.
Clinical Manifestations

● Preclinical AD, begins near the hippocampus, a

structure essential to the formation of short and long
term memories

● 10-20 years perhaps lead to memory loss

Clinical Manifestations
Mild Alzheimer's Disease

● the cerebral cortex begins to shrink

● memory disturbance

● poor
judgment and
problem solving
skills ● careless
in work habits
and household
chores ● may
become
confused
● agitation, apathy, dysphoria, aberrant motor behavior
Clinical Manifestations
Moderate Alzheimer's Disease

● demonstrate language disturbance characterized by

impaired word finding and circumlocution

● spontaneous speech becomes empty

● Paraphasias
● may repeat words and phrases spoken by themselves
(palalia) or by others (echolalia)
Clinical Manifestations
Moderate Alzheimer's Disease

● apraxia, inability to perform purposeful movement, not

related to paralysis ● restlessness with frequent pacing
● hyperorality

● swallowing may become difficult

● depression and irritability may worsen

● delusions and psychosis may appear

Clinical Manifestations
Severe Alzheimer's Disease

● Plaques and tangles are

widespread throughout the brain ●
Clients cannot recognized family
and friends ● Do not
communicate in any way
● Voluntary movement is minimal

● Limbs become rigid with flexor posturing

● Urinary and fecal incontinence

● Aspiration and aspiration pneumonia are frequent

Diagnostic Findings
● No definitive test for AD, diagnosis is made by exclusion of
known causes of dementia

● CT scan to identify ventricular dilation, sulcal

enlargement and cerebral atrophy

● MRI, PET to detect changes in brain function

● laboratory studies – CBC, urinalysis, BUN, creatinine,

thyroid values, liver function tests, syphilis serology,
HIV testing
Medical Management:
Pharmacologic● To
maintain mental
function:
● donepezil (Aricept)

● rivastigmine (Exelon)

● memantine (Namenda)
 ● tacrine (Cognex)

● galanthamine (Reminyl)

● these
drugs are
used to
maintain
memory
● To
control
depressi
on and
agitation
:
● Risperdal, Zyprexa, Seroquel, Zoloft
Nursing Diagnoses
and Interventions●
Impaired verbal
communication
● Impaired memory

● Risk for injury

● Self-care deficit

● Impaired nutrition: less

than the body
requirements

● Urinary and Fecal

incontinence
● Caregiver role strain

Parkinson’s Disease
Parkinson's Disease

● a chronic, progressive, neurologic disorder that results from

the loss of neurotransmitter DOPAMINE in a group of
disorder that control movements

● common in older population

● 60s but may strike in younger individuals

● not an inherited disease

Parkinson's Disease

● Dopamine, a chemical substance that enables people to

move normally and smoothly.
● When PD occurs, degenerative changes are found in
an area of the brain known as substantia nigra,
which produces dopamine.

● Once cell loss in substantia nigra reaches 50-80%, manifestations

occur.
Stage
s of
Parkinso
n's
DiseaseS
tage I

● symptoms affect only

one side of the body ●
mild, patient may not be
aware of symptoms ●
typical motor symptoms:
tremors and shaking
limbs ● family may
noticed tremor, poor
posture, mask face
Stages of Parkinson's Disease

Stage II

● symptoms begin affecting both sides of the body

● trouble walking and maintaining balance while standing

● increase difficulty performing once easy tasks: bathing,
cleaning, dressing ● still some patients lead a normal life
● may begin taking medications
Stages of Parkinson's Disease

Stage III

● Symptoms are more pronounced but can still function

without assistance ● obvious difficulty in standing, walking
and other physical movements ● likely to fall, but some
may perform independently
● Moderate stage
Stages of Parkinson's Disease

Stage IV

● symptoms are severe and disabling often needs assistance to

walk, stand and move
● motor symptoms: rigidity and bradykinesia are visible

● most cannot live alone

● Advanced stage
Stages of Parkinson's Disease

Stage V

● symptoms are most severe that require to be wheelchair-bound

or bedridden ● may not be able to perform movement without
assistance ● quality of life declines rapidly
● complications: infection, pneumonia, falls, choking

● with treatment may still live just like those without the disease
Clinical Manifestations

● Tremors at rest, pill rolling type, the first manifestation in

70% of the clients ● Rigidity, increased tone and stiffness of
the muscle at rest ● Bradykinesia (slow movement), fine
movements become clumsy ● Postural changes: flexed
posture of the neck, trunk, limb
Other Manifestations:
● slowing of ADLs, early of the disease tends to shuffle and
exhibits decreased arm swing

● as dexterity declines, micrographia develops

● stiff, mask-like without expression of the face during the advanced

PD

● speech is low, monotonous tone and slow (dysphonia),

words are poorly articulated (dysarthria)

● saliva flow involuntarily

● fatigue is common

● sleep disturbance

● low gastric motility - constipation

Other Manifestations:
● episodes of depression in 50% of clients

● usually does not affect intellectual ability

● dementia affects up to 70% of patients over the course of the

disease
● the course is slowly, PROGRESSIVE, the person
becomes more rigid, more disabled, requiring a full
assistance in ADLs
Assessment and Diagnostic Findings

● ongoing research with PET and CT scan has been helpful in

understanding the disease

● the disease is diagnosed from the patient's history and

presence of two of four cardinal manifestations: tremor,
rigidity, bradykinesia, and postural changes
Medical Management
● directed toward controlling symptoms and
maintaining functional independence

● no medical and surgical approaches currently use

to prevent disease progression

● antiparkinsonian medications act by increasing striatal dopaminergic

activity

● Levodopa is the most effective agent, it is converted to

dopamine in the basal ganglia, producing symptom relief

● Carbidopa is often added to avoid metabolism of

levodopa before it can reach the brain

● Sinemet (Levodopa/carbidopa)
Medical Management
● the beneficial effects levodopa are most pronounced in the
first year to two of treatment

● benefits begin to wane, and adverse effects become more severe

over time

● confusion, hallucinations, depression, and sleep alterations

are associated with prolonged use

● in 5-10 years, dyskinesia (impaired ability to execute voluntary

movements)
Nursing Interventions
● Stretching and Range of motion exercises to promote join flexibility.

● Warm baths and Massage to help relax muscles and

relieve painful muscle spams that accompany rigidity.

● Special walking techniques to offset the shuffling gait and

the tendency to lean forward.

● Perform breathing exercises while walking to help move

ribcage and aerate parts of the lungs.
● Frequent rest periods to aid in preventing frustrations and fatigue.