Infections of the Nervous System
Kathy Baule RN, MSN, APN, CNSBC-CCRN, CNRN, RNFA
Brain Abscess
• Pathogenic– can happen in any individual
• Opportunistic—can happen in individuals
with a compromised immune system
Abscesses--Incidence
•
•
•
•
•
Is 1-2% of SOL in brain (USA)
Is 8% (INDIA)
Antibiotic have helped change the incidence
Lastly increased incidence because of opportunistic
infection in immune compromised patient .
http://www.medicalnewstoday.com/articles/185614.php
Risk Factors
• Congenital heart disease
• Pulmonary AVM and AVFs as seen in hereditary
hemorrhagic telangiectasia (HHT)
• Bacterial Endocarditis (IV drug abuse)
• Lung Infections
Lung abscess
Bronchiectasis
Empyema
• Dental Abscess
• Systemic Sepsis
Brain Abscess
•Microorganism from remote site of infection
•Multiple and deeply located
•Mostly located in the frontal and parietal lobe
•Primary include skin pustule, pulmonary infection,
diverticulitis
•Most common type of CHD
•Brain abscess in CHD are generally solitary
Penetrating trauma :
Penetrating trauma are seen occur soon or after years
from trauma. Contaminated bone fragments and debris
provide a nidus for infection (A nidus is a breeding
place where bacteria, parasites, and other agents of a
disease lodge and develop)
Sharp Stabbing Headache
Penetrating Injury with Retained Object
Penetrating Injury with Retained Object
Brain Abscess
Amyotrophic Lateral Sclerosis
Disrupts the function of the motor neurons causing:
• Rapid progression of weakness
• Muscle atrophy
• Muscle spasticity
• Dysarthria (problems speaking)
• Dysphasia (problems swallowing)
• Dyspnea (problems breathing)
Amyotrophic Lateral Sclerosis
Pathology
• Degeneration and death of motor nerves
▫ Upper Motor Neuron
 within brain/spinal cord
▫ Lower Motor Neurons
 leaves brain (stem)/spinal cord
• Relatively spared
▫ Eye movements and bowel/bladder function
Motor Neuron Disease
Terminology
Lower motor neuron
Progressive
Muscular
Atrophy
Upper motor neuron
Amyotrophic Primary
Lateral
Lateral
Sclerosis
Sclerosis
Amyotrophic Lateral Sclerosis
Clinical Presentation
• Asymmetric Weakness – most common
• Onset single limb or bulbar
• Local spread then regional spread
▫ Bulbar, cervical, thoracic, lumbosacral
• Fasciculations
Amyotrophic Lateral Sclerosis
• Amyotrophic lateral sclerosis (ALS) is a rapidly
progressive, invariably fatal neurological disease
that attacks the nerve cells (neurons)
• Responsible for controlling voluntary muscles
(muscle action we are able to control, such as
those in the arms, legs, and face).
• The disease belongs to a group of disorders
known as motor neuron diseases, which are
characterized by the gradual degeneration and
death of motor neurons.
Amyotrophic Lateral Sclerosis
Diagnosis
• Two experienced Neurologists
Laboratory Studies
No study to prove or disprove
Look for an alternate diagnosis
Amyotrophic Lateral Sclerosis
Prognosis
• Variable – difficult to predict in an
individual patient
• 50% live 3-4 or more years
• 20% live 5 or more years
• 10% live 10 or more years
• Occasional patients live 20 years
Amyotrophic Lateral Sclerosis
Treatment
• Bulbar onset
▫ Prolonged survival
▫ Improved muscle strength
• Entire population
▫ Prolonged survival
▫ No effect on effect on decline in muscle
strength
• Prolonged survival an average of 2-3
months
AIDS
• HIV is a virus spread through body fluids that affects
specific cells of the immune system, called CD4
cells, or T cells. Over time, HIV can destroy so many
of these cells that the body can’t fight off infections
and disease. When this happens, HIV infection leads
to AIDS.
Anyone Can Get HIV
• The Centers for Disease Control (CDC) estimates 1.1
million people age 13 and older are infected with
HIV, and 50,000 people are newly infected each year.
Anyone can be infected with HIV.
• In 2010, men who have sex with men accounted for
63% of new infections, and women accounted for
20% of new infections. The incidence of HIV among
African-Americans is about 8 times as high as in
whites.
•
http://www.cdc.gov/hiv/library/factsheets/index.html
You Can Have a Baby if You Are HIVPositive
• Pregnant women who are HIV positive can pass
the HIV virus to their babies. It can happen
during pregnancy, during vaginal childbirth, or
while breastfeeding.
• However, if the mother receives treatment with
antiretroviral drugs during pregnancy, has a Csection delivery, and avoids breastfeeding, she
can greatly reduce the risk of passing the
infection on to her baby.
•
http://www.cdc.gov/hiv/library/factsheets/index.html
HIV-Infected patients
• Dementia
• Cerebral signs and symptoms are the most
common
• Global cerebral disease can present with altered
mental status or generalized seizures
• Whereas focal disease often produces
hemiparesis, hemisensory loss, visual field cuts,
or disturbances in language use.
HIV-Infected Patients
• Fungal, viral, and mycobacterial
meningoencephalitides are the most common causes
of global cerebral dysfunction, and progressive
multifocal leukoencephalopathy (PML), primary
CNS lymphoma, and toxoplasmosis account for the
majority of focal presentations.
•
http://hivinsite.ucsf.edu/InSite?page=kb-04-01-02#S1.1X
HIV
• Availability of effective antiretroviral regimens has
been associated with a dramatic decline in incidence
and severity of opportunistic infections of the CNS.
• Unfortunately, antiretroviral regimens have not
demonstrably decreased the prevalence of PML, and
the incidence among individuals with higher CD4
counts may be increasing.
• The prognosis has improved dramatically, with
long-term remissions now fairly common among
patients receiving antiretroviral therapy.
•
http://hivinsite.ucsf.edu/InSite?page=kb-04-01-02#S1.1X
Bell’s Palsy
•
WHAT IS BELL'S PALSY?
Bells palsy is a condition that causes the facial muscles to weaken or become paralyzed. It's caused by trauma to
the 7th cranial nerve, and is not permanent.
•
WHY IS IT CALLED BELL'S PALSY?
The condition is named for Sir Charles Bell, a Scottish surgeon who studied the nerve and its innervation of the
facial muscles 200 years ago.
•
HOW COMMON IS BELL'S PALSY?
Bells palsy is not as uncommon as is generally believed. Worldwide statistics set the frequency at just over .02% of
the population (with geographical variations). In human terms this is 1 of every 5000 people over the course of a
lifetime and 40,000 Americans every year.
•
IS BELL'S PALSY ALWAYS ON THE SAME SIDE?
The percentage of left or right side cases is approximately equal, and remains equal for recurrences.
•
IS THERE ANY DIFFERENCE BECAUSE OF GENDER OR RACE?
The incidence of Bells palsy in males and females, as well as in the various races is also approximately equal. The
chances of the condition being mild or severe, and the rate of recovery is also equal.
Bell’s Palsy
• Sudden weakness of half of the face
• The smile is one-sided and the eye on the weak
side resists closing.
Bell’s Palsy’s Causes
• Unknown Causes
• Believed to be a result of swelling and
inflammation of the nerves that control the
muscles
• Could be a reaction that occurs after a viral
reaction
Facial Nerve
• Controls the muscles on one side of the face
• Difficulty blinking, closing and facial expression
such as smiling and frowning
• Other symptoms include drooping of the eyelid and
corner of the mouth, drooling, dryness of eye or
mouth, impairment of taste and excessive tearing in
one eye
Bell’s Palsy Case Study
•
C.B., is a 19 year old female university student with complaints of dry left eye. She had taken out
her contacts and supplemented the dryness with saline drops. As the time progressed over night
he had noticed difficulty blinking with pain in the left ear. He had developed complete left facial
paralysis. The symptoms began in August and with gradually recovery beginning two months post
onset. She was seen by a Neurologist who confirmed the diagnosis of Bell’s palsy.
•
She was referred for facial neuromuscular retraining nine months post onset of symptoms. Initial
evaluation revealed slightly increased resting tone, complete eye closure, slightly decreased smile
with mild synkinesis noted. Attempted lip movements were accompanied by severe synkinesis of
orbicularis oculi which resulted in almost complete eye closure (Figures 5, A-D).
•
The home program consisted of small selective movements practiced with inhibition of
synkinesis. She attended clinic sessions once a month for the first six months and demonstrated a
significant reduction in synkinesis during that time (Figures 5, E-H). Clinic visits decreased to
once every three months with continued good compliance. The entire course of neuromuscular
retraining lasted 18 months with improvements noted in volitional and spontaneous excursion of
movement. The patient continued to demonstrate mild synkinesis of orbicularis oculi during
broad, spontaneous laughter. She was extremely motivated and compliant with the home
program, and was pleased with the treatment outcome.
Photographic evaluation 12
months post left facial paralysis
resulting
Pre-treatment: Resting tone (A), smile
(B), pucker (C), pout (D). Note normal
resting tone, decreased excursion of left
smile with mild synkinesis of left
OCS/OCI and severe synkinesis of left
OCS/OCI during lip movements.
Reevaluation of same movements six
months after beginning facial NMR (EH). Note improved excursion of smile
and decreased synkinesis around eye
with improved symmetry.
Encephalitis
• Most diagnosed cases of encephalitis in the United States
are caused by enteroviruses, herpes simplex virus types 1
and 2, rabies virus (this can occur even without a known
animal bite, such as for example due to exposure to bats),
or arboviruses such as
• West Nile virus, which are transmitted from infected
animals to humans through the bite of an infected tick,
mosquito, or other blood-sucking insect.
• Lyme disease, a bacterial infection spread by tick bite,
more typically causes meningitis, and rarely encephalitis.
Encephalitis: Symptoms
• Fever, headache, seizures, change in behavior or
confusion and in extreme cases, brain damage, stroke
or even death
• Infection of the meninges, the membranes that
surround the brain and spinal cord
Infectious Causes
• Bacteria, viruses, fungi and parasites
• Many of these affect healthy people
• For others, environmental and exposure history,
recent travels or immunocompromised states
(HIV, diabetes, steroids and chemotherapy)
• Non-infectious causes: autoimmune causes and
medication
Treatment for mild cases
•
•
•
•
Can be mistaken as the flu, mainly consists of:
Bed rest
Plenty of fluids
Anti-inflammatory drugs— such as acetaminophen (Tylenol,
others), ibuprofen (Advil, Motrin IB, others) and naproxen
sodium (Aleve, others) — to relieve headaches and fever.
• Antiviral drugs
• Cases due to certain viruses usually require intravenous
antiviral treatments.
• Antiviral drugs commonly used to treat encephalitis include:
▫ Acyclovir (Zovirax)
▫ Ganciclovir (Cytovene)
▫ Foscarnet (Foscavir)
Demyelinating Polyneuropathy
Guillain-Barre
• Guillain-Barre: is an acute inflammatory disease of
the peripheral nerves. An autoimmune attack on the
myelin (insulation around individual nerve fibers,
called axons) results in demyelination. Loss of
myelin can occur in sensory, motor or autonomic
nerves.
GB
• After the first clinical manifestations of the
disease, the symptoms can progress over the
course of hours, days, or weeks. Most people
reach the stage of greatest weakness within the
first 2 weeks after symptoms appear, and by the
third week of the illness 90 percent of all
patients are at their weakest.
•
http://www.medicinenet.com/guillain-barre_syndrome/page2.htm
GB
• Approximately one third of patients require
admission to an ICU, primarily because of
respiratory failure.
• After medical stabilization, patients can be treated
on a general medical/neurologic floor, but
continued vigilance remains important in
preventing respiratory, cardiovascular, and other
medical complications.
• Patients with persistent functional impairments may
need to be transferred to an inpatient rehabilitation
unit.
GB Treatment
• Immunomodulatory treatment has been used to
hasten recovery. Intravenous immunoglobulin
(IVIG) and plasma exchange have proved
equally effective.
• Corticosteroids (oral and intravenous) have not
been found to have a clinical benefit in GBS.
• Consequently, this class of drugs is not currently
employed in treatment of the syndrome.
•
http://emedicine.medscape.com/article/315632-treatment
Demyelinating Polyneuropathy
CIDP
• Chronic Inflammatory Demyelinating
Polyneuropathy(CIDP) is a neurological disorder
characterized by progressive weakness and
impaired sensory function in the legs and arms.
The disorder, which is sometimes called chronic
relapsing polyneuropathy, is caused by damage
to the myelin sheath (the fatty covering that
wraps around and protects nerve fibers) of the
peripheral nerves
CIPD
• Is common in young adults and is more
prevalent in males
• Presents with numbness and tingling beginning
in the toes and the fingers, weakness in the arms
and legs; loss of deep tendon reflexes; fatigue
and abnormal sensations
CIPD
• 51-year-old female who has been treatment for GuillainBarre and CIDP. Her symptoms began on June 2001.
She was having fatigue episodes with associated lower
extremity weakness. The weakness was progressive in
nature until she reached a point that she could not walk.
She has chronic weakness in the bilateral lower
extremities with associated numbness, tingling, and
burning pain.
• She is under the care at the Mayo Clinic. Her pain
management regimen is currently controlling her
discomfort at a level she can complete her activities of
daily living with periods of rest. She denies any bowel or
bladder incontinence, but has been treated for
diverticulitis.
CIPD
• She received IVIG weakly and Cellcept
• She has areas of numbness and tingling and
chronic pain issues. She is stable on MSIR and
Lyrica
• She continues to have numbness, tingling and
burning pain
• She has an ataxic gait, but is able continue her
activities of daily living and is currently baby
sitting daily.
Demyelinating Polyneuropathy
ADEM
• Is a rare inflammatory demyelinating disease of
the central nervous system. ADEM is thought to
be an autoimmune disorder in which the body’s
immune system mistakenly attacks its own brain
tissue, triggered by an environmental stimulus
in genetically susceptible individuals.
ADEM
• The diagnosis of ADEM is based on clinical and
radiologic characteristics.
• There is no specific biologic marker or
confirmatory test to specifically identify the
disorder
• There is no scientific, randomized, or controlled
data on the diagnosis and treatment of ADEM.
• Decisions about the diagnosis and treatment of
this disorder are based primarily on the opinions
of experts
http://myelitis.org/symptoms-conditions/acute-disseminated-encephalomyelitis/diagnosis/
ADEM
• Post-infectious In approximately 50-75 percent of
ADEM cases, the inflammatory attack is preceded by a
viral or bacterial infection.
• There have been a large number of viruses associated
with these infections, including but not limited to:
measles, mumps, rubella, varicella zoster, Epstein-Barr,
cytomegalovirus, herpes simplex, hepatitis A, influenza,
and enterovirus infections.
• A seasonal distribution has been observed showing that
most ADEM cases occur in the winter and spring. The
inflammatory attack and neurological symptoms often
begin within a couple of weeks after the viral or bacterial
illness. http://myelitis.org/symptoms-conditions/acute-disseminated-encephalomyelitis/
ADEM
• Considered when individuals develop multifocal
neurologic abnormalities with confusion, excessive
irritability, or altered level of consciousness
(encephalopathy)
• Especially if the onset of symptoms occurs within 1 to 2
weeks after a viral/bacterial infection or a vaccination.
• Must rule out that there is a direct infection of the
central nervous system as opposed to an infection that
subsequently triggered the immune system to cause the
attack
• Should a direct infection be suspected, one is often
placed on an antibiotic and/or acyclovir (an antiviral
drug) to fight the infection http://myelitis.org/symptoms-conditions/acute-disseminatedencephalomyelitis/diagnosis/
Lumbar Puncture/ ADEM
• This test is useful because evidence of
inflammation is common in cerebrospinal fluid
(CSF), with pleocytosis (increased white blood
cell count) and/or increased protein
concentration.
• While this is common, sometimes the CSF can
be normal. Additionally, although oligoclonal
bands are nonspecific and are more often
associated with Multiple Sclerosis (MS), they are
sometimes also present in ADEM.
http://myelitis.org/symptomsconditions/acute-disseminated-encephalomyelitis/diagnosis/ etimes also present in ADEM.
MRI of the Brain and Spine
• Abnormalities are best defined by T2-weighted images, FLAIR
sequences, and contrast-enhanced MRI with gadolinium.
Abnormalities on MRI usually vary in location.
• Lesions associated with ADEM tend to be bilateral, but can also be
asymmetric and are typically poorly marginated.
• Multiple lesions in the deep and subcortical white matter are
common, which is characteristic of demyelination (gray matter
lesions sometimes accompany white matter lesions, especially
among children).
• While the number varies, multiple brain lesions are usually present.
ADEM lesions are typically large (though smaller ones have also
been seen) with diameters ranging from <5 mm to 5 cm.
Additionally, brainstem and spinal cord abnormalities on MRI are
common in ADEM.
• In the spinal cord, there are typically large confluent intramedullary
lesions that extend over multiple segments of the cord.
MRI
• In a situation where nonspecific cerebrospinal
fluid abnormalities and MRI evidence of white
matter lesions are present, it is important that
other inflammatory demyelinating disorders be
considered.
• These include: Multiple Sclerosis Multiple (MS),
Optic Neuritis Optic (ON), Transverse Myelitis
(TM), and Neuromyelitis Optica (NMO).
Treatment
• IV Corticosteroids are the most common treatment for ON.
Or high dose tablets. While corticosteroids have been effective
in improving short-term visual recovery, they do not seem to
affect the long-term outcome.
• Lack of long-term benefit and the risk of potential side effects
(including: insomnia, weight gain, and mood alterations), the
use of corticosteroids is usually not advised.
• However, there are specific situation period of impairment
and are usually considered when a more rapid recovery is
required (such as patients with severe bilateral visual loss or
those with occupations that require normal visual acuity).
• Unfortunately, there are currently no acute treatments that
can reverse vision loss caused by ON. http://myelitis.org/symptoms-conditions/opticneuritis/acute-treatments-on/
Meningitis
• Meningitis is a disease caused by the
inflammation of the protective membranes
covering the brain and spinal cord known as the
meninges. The inflammation is usually caused
by an infection of the fluid surrounding the brain
and spinal cord.
Meningitis
• Bacterial meningitis is usually severe. While most people
with meningitis recover, it can cause serious
complications, such as brain damage, hearing loss, or
learning disabilities.
• There are several pathogens (types of germs) that can
cause bacterial meningitis. Some of the leading causes of
bacterial meningitis in the United States include
Haemophilus influenzae (most often caused by type b,
Hib), Streptococcus pneumoniae, group B
Streptococcus, Listeria monocytogenes, and Neisseria
meningitidis.
• In the United States, about 4,100 cases of bacterial
meningitis, including 500 deaths, occurred each year
between 2003–2007.
Viral Meningitis
• Meningitis is an inflammation of the tissue that
covers the brain and spinal cord.
• Viral meningitis is the most common type of
meningitis
• Often less severe than bacterial meningitis
• People usually get better on their own
• However, infants younger than 1 month and
people with weakened immune systems are
more likely to have severe illness
Myasthenia Gravis
• Myasthenia gravis is a disease of skeletal muscle acetylcholine
receptors. The chemical transmitter, acetylcholine (ACh) is
unable to bind to the receptors (AChR) on the postsynaptic
membrane to transmit the nerve impulse to muscle fibers to
produce a muscle contraction
Myasthenia gravis is a disease of skeletal muscle
acetylcholine receptors. The chemical transmitter,) is
unable to bind to the receptors (on the postsynaptic
membrane to transmit the nerve impulse to muscle fibers
to produce a muscle contraction
severe with marked bulbar
involvement
Myasthenia Gravis
• 64 year old female developed sudden on-set of left
eye double vision and weakness in BLE. She was
seen by local Neurologist without a definitive
diagnosis.
• Tensilon test: The test helps:
• Diagnose myasthenia gravis
• Tell the difference between myasthenia gravis and
other similar brain and nervous system conditions
• Monitor treatment with oral anticholinesterase
drugs
MG
• She has notable ptosis ("drooping") of both eyelids after
repeated blinking exercises. When smiling, she appears
to be snarling.
• Electromyographic testing revealed progressive
weakness and decreased amplitude of contraction of the
distal arm muscles
• Both her symptoms and electromyographic findings
were reversed within 40 seconds of intravenous
administration of edrophonium (Tensilon), an
acetylcholinesterase inhibitor (i.e. an
"anticholinesterase").
• Blood testing revealed high levels of an antiacetylcholine receptor antibody in her plasma, and a
diagnosis of myasthenia gravis was made.
Myasthenia Gravis
• There is no known cure for MG, but there are
effective treatments available. Common
treatments include medications, thymectomy
and plasmapheresis. Spontaneous improvement
and even remission may occur without specific
therapy.
• She was treated with steroids, Imuran and
Methotrexate
• She is currently taking Rituxan (4 doses IV every
two years); she is weaning her steroids.
MG
• She was treated with with pyridostigmine bromide,
which is a long-acting anticholinesterase drug, and
was also started on prednisone, which is a
corticosteroid drug.
• She also underwent occasional plasmapheresis when
her symptoms became especially severe.
• She was given a prescription of atropine as needed
to reduce the nausea, abdominal cramps, diarrhea,
and excessive salivation she experienced as side
effects of the anticholinesterase drug.
Multiple Sclerosis
• Is a disease with unpredictable symptoms that
can vary in intensity. While some people only
have fatigue and numbness, severe cases can
cause paralysis, vision loss, and diminished
brain function.
• MS affects about 2.5 million people worldwide
and affects women twice as often as men
(National MS Society, 2012).
MS
• In multiple sclerosis (MS), damage to the myelin
coating around the nerve fibers in the central
nervous system (CNS) and to the nerve fibers
themselves interferes with the transmission of
nerve signals between the brain, spinal cord and
the rest of the body.
• Disrupted nerve signals cause the symptoms of
MS, which vary from one person to another and
over time for any given individual, depending on
where the damage occurs.
MS
• Types of MS. Four disease courses have been
identified in multiple sclerosis: relapsingremitting MS (RRMS),
• primary-progressive MS (PPMS),
• secondary-progressive MS (SPMS), and
• progressive-relapsing MS.
• Each of these disease courses might be mild,
moderate or severe.
MS treatment
• Treatments for signs and symptoms
• Physical therapy. A physical or occupational therapist can
teach you stretching and strengthening exercises, and show
you how to use devices that can make it easier to perform
daily tasks.
• Muscle relaxants. You may experience painful or
uncontrollable muscle stiffness or spasms, particularly in your
legs. Muscle relaxants such as baclofen (Lioresal, Gablofen)
and tizanidine (Zanaflex) may help.
• Medications to reduce fatigue.
• Other medications. Medications may also be prescribed for
depression, pain, and bladder or bowel control problems that
are associated with MS.
•
Prion Disease
• Prion diseases or transmissible spongiform
encephalopathies (TSEs) are a family of rare
progressive neurodegenerative disorders that affect
both humans and animals. They are distinguished by
long incubation periods, characteristic spongiform
changes associated with neuronal loss, and a failure
to induce inflammatory response.
• CJD
Encephalopathy
• Disease, damage, or malfunction of the brain. In
general, encephalopathyis manifested by an
altered mental state that is sometimes
accompanied by physical changes.
• Toxic
• Metabolic
• PRESS
PRES Presentation
• Patients present with headache, seizures,
encephalopathy and/or visual disturbance.
PRES
• Most commonly there is vasogenic oedema within the
occipital and parietal regions (~95% of cases), perhaps
relating to the posterior cerebral artery supply.
• The oedema is usually symmetrical. Despite being
termed posterior,
• PRES can be found in a non posterior distribution,
mainly in watershed areas, including within the frontal,
inferior temporal, cerebellar and brainstem regions
• There are three main imaging patterns:
• holohemispheric at watershed zones
• superior frontal sulcus
• parieto-occipital dominance http://radiopaedia.org/articles/posterior-reversibleencephalopathy-syndrome-1
PRES
• PRES is reversible when treatment is instituted
early, delayed diagnosis and treatment can result in
chronic neurological sequelae.
• Early recognition and controlled of blood pressure
and seizure is the main stay of treatment.
• Anesthesiologist, intensivists and other physicians
involved in the evaluation of patients with markedly
elevated blood pressure, eclampsia, renal failure etc
should presumed PRES and must be aware of the
clinical spectrum of the associated conditions, its
diagnostic modalities, and treatment.
Thank you!!