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Cerebritis Symptoms and Treatment Alternatives

Cerebritis is a medical term referring to the inflammation of the brain tissue and as the swelling caused by the
inflammation grows, the patient may experience different cerebritis symptoms. Cerebritis is caused by
infections in the brain and it is mainly a symptom itself.
Although the main cause of cerebritis is infections, patients with lupus (an autoimmune inflammatory disorder)
frequently develop a certain degree of inflammation of the brain tissue. Lupus can cause other symptoms such
as red patches on the cheeks which may also extend to the rest of the face, neck and other parts of the body.
Discoid lupus is a condition that only affects the skin. Systemic lupus on the other hand, is a condition that can

cause sudden symptoms or symptoms that develop over months or years. Commonly, systemic lupus is
signaled by chronic fatigue.
It is estimated that more than half of the patients with lupus from the United States suffer from a degree or
another of lupus cerebritis.
An accurate lupus cerebritis diagnosis must be established prior to following a specific treatment plan. The
lupus cerebritis diagnosis is quite difficult to make. The disease can result in mild to severe symptoms which
include headaches, seizures, stroke, dementia, peripheral neuropathy, cerebellar ataxia (the inability to
coordinate the muscles, usually on one side of the body), chorea (involuntary movements), psychosis, and
others. However, laboratory tests and imaging tests can help in diagnosing the condition.
Before starting the cerebritis treatment, it is important to accurately establish what causes the inflammation in
the first place. Cerebritis is not only a result of lupus but it can be caused by a wide range of infections that
either start in the brain or travel to the brain through blood. Brain inflammation can be a result or either bacterial
infection such as meningitis or fungal infections. The first is mainly treated with broad spectrum antibiotics while
the latter is cured with antifungal medication. Cerebritis treatment varies based several factors including the
age of the patient, the general health condition of the patient, the specific type of disease that is causing the
inflammation and the severity of the disease. For example, cerebritis may lead to brain abscesses which are
medical emergencies and which are treated with antibiotics or antifungal drugs or surgery. In this particular
case, surgery may remove that abscess but only if it is not too deep in the brain and if it is not too large. Thus,
so many factors must be taken under consideration when establishing a specific treatment schema for a patient
wit cerebritis.
Cerebritis is however a severe medical condition. As the symptoms evolve and worsen, patients may develop
severe and life-threatening conditions such as heart-related death-causing diseases or stroke or coma. It is
recommended that patients who experience sudden symptoms of cerebritis are brought to the nearest hospital
as soon as possible.
As a conclusion, cerebritis symptoms may develop gradually and that makes it difficult to recognize them in the
first place but given the severity of the condition, anyone who is at risk of developing it must be aware of them.

Cerebritis is an infection of the brain that normally leads to the formation of an abscess within
the brain itself. Cerebritis is an inflammation of the cerebrum, a structure within the brain which
performs a number of important functions, including most of the things which people associate
with being human, such as memory and speech.[1] It is also defined as a purulent nonencapsulated
parenchymal infection of brain which is characterized by nonspecific features on CT (ill-defined
low density area with peripheral enhancement) and cannot reliably be distinguished from
neoplasms.[2]
Cerebritis usually occurs as a result of an underlying condition, which causes the inflammation
of the brain tissue. It is commonly found in patients with lupus.
Lupus cerebritis may occur in adults and children. The duration of the central nervous system
involvement may vary from a few minutes, as in classic migraine or a transient ischemic attack,
to years, as in dementia. Resulting neurological deficits may be transient or permanent,
occasionally resulting in death.[3]
Contents
[hide]

1 Symptoms

2 Causes

3 Treatment

4 References

[edit] Symptoms

The symptoms of cerebritis may range from mild to severe.[4]

The severity of the symptoms varies based on the degree of swelling and on how elevated is the
intracranial pressure. Mild symptoms include headaches, depression, anxiety and in some cases,
memory loss. In some cases inflammation of brain can be seen if the brain or the nervous system
is attacked as a result of problems with the immune system. The serious problems caused
because of inflammation include headaches, seizures, vision problems, dizziness, behavior
changes and even stroke.[5]
Severe lupus cerebritis symptoms include psychosis, dementia, peripheral neuropathy, cerebellar
ataxia (failure of muscular coordination, usually on one side of the body), and chorea (jerky,
involuntary movements). Stroke incidence is 3-20% in systemic lupus patients, and is highest in

the first five years of the disease. Peripheral neuropathy (carpal tunnel syndrome, for example)
occurs in more than 20% of systemic lupus patients and cranial nerve palsies occur in 10-15%.[6]
[edit] Causes

Lupus systemic erythematosus is one of the most common causes of cerebritis as it is believed
that more than half of the patients with lupus from the United States suffer from a degree or
another of lupus cerebritis.[7]
The exact pathophysiological process of lupus cerebritis is unknown. The proposed mechanisms
are likely due to the assault of several autoimmune system changes, including the following:

Circulating immune complexes. The immune complexes, which consist of DNA

and anti-DNA, cause an inflammatory response as well as a disruption of the
blood-brain barrier. These circulating complexes have been found trapped in
the highly vascular choroid plexus of SLE patients upon autopsy. True
vasculitis, however, is found only in about 10% of patients with cerebral
lupus.[8]

Anti-neuronal antibodies. The three identified anti-neuronal antibodies

postulated in CNS involvement are the lympho-cytotoxic antibodies (LCAs),
which somehow react with brain tissue and interfere with the neuron's ability
to respond. LCAs have a specific role and are found in both the serum and
cerebrospinal fluid (CSF) of lupus patients with cerebritis. These antibodies
also correlate with cognitive and visual spatial defects. Second, the antineuronal membrane antibodies are targeted directly to neuronal antigens.
They, too, are found in the serum of SLE patients with cerebritis. And third,
the intracytoplasmic antibodies target the constituents of the neuron cells
and they are found in the CSF and serum. These antibodies are seen in 90%
of SLE patients with psychosis.[9]

Antiphospholipid antibodies. The two antibodies implicated are anticardiolipin

and lupus anticoagulant. Anticardiolipin antibodies attach to the endothelial
lining of cells, causing endothelial damage, platelet aggregation,
inflammation, and fibrosis.[10]

Cytokine release. The final mechanism of lupus cerebritis involves the

cytokines. The cytokines trigger edema, endothelial thickening, and
infiltration of neutrophils in brain tissue. Two cytokines, interferon alfa and
interleukin-6, have been found in the CSF of SLE patients with psychosis. [11]

However, it is not clear which mechanism is the actual cause of cerebritis in lupus patients.
Specialists believe that all mechanisms may be present at the same time or they may act
independently.
In very rare cases, cerebritis may occur as a result of a Klebsiella pneumoniae infection.[12]

One other reason to develop cerebritis is an infection caused by bacteria, viruses, or other
organisms. Infections can occur when infectious agents enter the brain through the sinuses or as a
result of trauma. Some pathogens are also capable of passing over the blood-brain barrier and
entering the brain through the bloodstream, despite the fact that the body has evolved defenses
which are specifically designed to prevent this.[13]
[edit] Treatment

Lupus is a condition with no known cure. Lupus cerebritis however is treated by suppressing the
autoimmune activity.[14]
When it is caused by infections, treatment consists of medication that will primarily cure the
infection. For inflammation, steroids can be used to bring down the swelling. If the swelling
appears to have increased to a dangerous level, surgery may be needed to relieve pressure on the
brain. The formation of an abscess also calls for surgery as it will be necessary to drain the
abscess.
Introduction
Background
The introduction of infectious agents results in various responses from the central nervous system (CNS). In
the earliest stage of purulent bacterial brain infection, the generalized initial reaction is cerebritis. Within the
background of cellular response to the infection, cerebritis evolves into a localized abscess in a predictable
series of stages. Neuroimaging of these stages reflects the underlying pathophysiology of abscess formation.
Variations in the brain's reaction at different locations and similarities in the brain's reaction to certain agents
and in the appearances of aggressive neoplasms all require correlation of medical history, neuroimaging, and
results of microbiologic analysis.
Early and improved diagnostic imaging techniques have allowed the discovery of brain abscess at a much
earlier stage. (See the images below.)

Brain abscess. Axial CT scan in a patient who presented with a headache, fever, and a
history of a recent pneumonia demonstrates a poorly defined area of posterior parietal
brain edema (arrows). Early cerebritis may not outline a focal mass clearly.

Brain abscess. Axial nonenhanced cranial CT scan in a patient who presented with fever,
headache, and a previous paranasal sinus infection demonstrates a poorly defined pattern
of mass effect and low attenuation in the left temporal lobe. The pattern is consistent with
possible early cerebritis; however, glioma and infarct may have similar presentations.

Brain abscess. Three-dimensional surface model of a cranial CT scan in a patient with a

postcraniotomy abscess. The large deformity in the skull indicates the route of abscess
spread.

Brain abscess. Axial T2-weighted MRI in a patient with a right frontal abscess. Note the
mass effect and surrounding edema. The wall of the abscess is relatively thin (black
arrows).

Preferred examination
The preferred initial examination of the patient in whom brain abscess is suspected is MRI with and without
gadolinium enhancement. Similar diagnostic results can be expected from cranial CT scans without and with
the intravenous administration of iodinated contrast medium. Both imaging techniques help detect the mass
effect of the abscess; however, findings in MRI with a diffusion protocol are more specific in differentiating
cerebral tumor, stroke, and abscess. In particular, examination of the metabolite peaks with MR spectroscopy
can help to specifically differentiate tumor, radiation necrosis, and abscess by identifying their different spectral
profiles.1,2

Perfusion MRI has also been used to differentiate these lesions by evaluating vascularity with blood flow
analysis with dynamic intravenous gadolinium contrast injection studies.
Occasionally, distinguishing brain abscess from neoplasm or postoperative changes from infection is difficult. In
these patients, a nuclear agent can be used to tag white blood cells or antibodies to help differentiation.
Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine
[MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have been
linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD).
For more information, see the eMedicine topic Nephrogenic Systemic Fibrosis. The disease has occurred in
patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to
enhance MRI or MRA scans.
NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin;
burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint
stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs;
and muscle weakness. For more information, see Medscape.
Limitations of techniques
Plain radiographs of the paranasal sinuses can only suggest a possible etiology for cerebral abscess. Early
findings of CT examinations are not specific for cerebral abscess. The edema pattern and moderate mass
effect cannot be differentiated from tumor or stroke in some patients. MRI findings in patients with cerebritis
may resemble findings in stroke, while findings in the infarcts that result from vasculitis and cerebritis may
resemble those of embolic strokes. Nuclear medicine single photon emission computed tomographic (SPECT)
findings are not specific for brain abscess unless a white cell tag is used.
Follow-up scans for certain infectious agents, such as M tuberculosis, may be necessary because infection by
these organisms may not follow a predictable response to treatment. Tuberculosis-related brain abscesses that
retain positive results to culture and smears following 4 weeks of treatment may not represent treatment failure.
In addition, treatment of fungal infections may require many weeks of treatment with interval follow-up imaging
studies. Follow-up imaging during the treatment for toxoplasmosis is important in avoiding brain biopsy.
Intervention
Intervention in patients with cerebral abscess is most commonly limited to biopsy and aspiration of infectious
material that may represent the origin of a CNS infection.
Aspiration and biopsy of small lesions is performed best using a CT-guided computer-assisted technique or
with the aid of an external frame, which (with the aid of CT data) directs the placement of the aspiration needle.
More recently, fully computer-aided virtual imaging programs have provided greater flexibility in the application
of both CT and MRI sets during craniotomy procedures and in the aspiration of selected lesions. Intraoperative
ultrasonography may aid in the detection and treatment of relatively large superficial abscess collections.
Recent studies
In a study by Chiang et al, diffusion, perfusion-weighted, and spectroscopic MRIs were able to differentiate
cerebral abscesses from necrotic tumors. The authors found that the mean apparent diffusion coefficient value

at the central cavities of the cerebral abscesses were significantly lower; the mean relative cerebral blood
volume values of the necrotic tumor walls were significantly higher; and amino acids were present only in the
cerebral abscesses.3
Sepahdari et al found that in 9 cases of orbital cellulitis, including 6 cases of pyogenic abscess, diffusionweighted imaging confirmed abscess in a majority of cases without contrast-enhanced imaging. According to
the authors, this may be of particular importance in patients in whom the use of contrast is contraindicated.
Diffusion-weighted imaging improved diagnostic confidence in virtually all the patients with orbital abscess
when it was used along with contrast-enhanced imaging. 4
For excellent patient education resources, visit eMedicine's Brain and Nervous System Center. Also, see
eMedicine's patient education article Brain Infection.

Brain Abscess
Author: Lisa Elizabeth Thomas, MD, Staff Physician, Harvard Affiliated Emergency Medicine Residency, Brigham and
Women's Hospital and Massachusetts General Hospital
Coauthor(s): Joshua N Goldstein, MD, PhD, FAAEM, Assistant Professor, Harvard Medical School; Attending Physician,
Department of Emergency Medicine, Massachusetts General Hospital
Contributor Information and Disclosures
Updated: May 13, 2010

Overview

Differential Diagnoses & Workup

Treatment & Medication

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References

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Introduction
Background

Although rare in developed countries, brain abscess is a serious, life-threatening emergency. Once having a
dire outcome, morbidity and mortality have decreased because of advances in diagnostic modalities, antibiotic
regimens, and earlier surgical interventions.1,2 However, changes in epidemiology, including new disease
pathogens and predisposing factors, have renewed concern about the diagnosis and treatment of this
condition.

Pathophysiology
Brain abscess is a focal infection, which begins when organisms are inoculated into the brain parenchyma,
usually from a site distant from the central nervous system (CNS). Abscess formation occurs through several
stages. Inflammation during the "early cerebritis" stage evolves into a necrotic collection of pus, eventually
surrounded by a well-vascularized capsule after 2 weeks.3,4
The 3 mechanisms of entry into the brain are as follows: 2,5,6

Direct extension: Infections stemming from the sinuses, teeth, middle ear, or mastoid may gain access
to the venous drainage of the brain via valveless emissary veins that drain these regions. Because of
improved antibiotic therapy for ear infections, this mechanism is decreasing in incidence, accounting
for only approximately 12-25% of cases.2,7 However, in developing countries, this is still a significant
source accounting for at least 50% of cases. 8

Hematogenous: Seeding of the brain occurs from distant infection sites and often results in multiple
brain abscesses.9 This remains an important cause of brain abscess.

Following penetrating head injury or neurosurgery: Previously low in incidence, more brain abscesses
are developing after head trauma and neurosurgical procedures. A case series found that 37% of brain
abscesses were associated with head penetration.2,10

Up to 30% of abscesses are cryptogenic and have no clear source. 2,8,9

Frequency
United States

Brain abscess is rare in the general population; however, immunocompromised patients have increasing
incidence of brain abscess, often with fungal or protozoan organisms.
In the United States, 1500-2500 cases are reported per year.9

Mortality/Morbidity

The mortality rate from brain abscess is currently approximately 10%. 1,2,8,11,12

However, if the abscess ruptures into the ventricular system, the mortality rate may be 80%. 2

Morbidity in survivors is generally due to residual neurologic defects, increased incidence of seizures
due to scar tissue foci, or neuropsychiatric changes. 9

Race

No compelling evidence exists for racial differences in the incidence of brain abscess.

Sex
Brain abscess occurs two to four times as often among men than women. 2,4,7,8,13,14

Age
Traditionally, brain abscesses were disproportionately diagnosed in the young. However, with changes in
vaccination practices, treatment of pediatric infections, and the AIDS pandemic, current literature suggests a
shift in peak incidence toward the third to fifth decades of life. 2,14,15 The minority of abscesses that do occur in
children peak in the age range of 4-7 years.16

Clinical
History

Headache is the most common presenting symptom of brain abscess (50-90% of cases). 2,7,14

Focal neurologic deficit (50%) may correlate with the local region of infection. 6,7

Classic triad of headache, fever, and focal neurologic deficit is rarely seen (<5-20% of cases in case
series).2,8

Seizure (40%) and mental status changes (50%) are common. 2,14

Nausea, vomiting, or stiff neck may be reported with increased cerebral edema due to the mass
lesion.6,8

Sudden worsening of a preexisting headache accompanied with meningismus may be indicative of a

catastrophic eventrupture of the abscess into the ventricular space. 6

Physical

Fever is typically low grade, but presence or absence of fever does not aid in diagnosis, as it is present
in less than half of all cases.6,14

Altered mental status ranges from subtle personality changes through drowsiness to full-blown coma. 14

Nuchal rigidity occurs in about 25% of cases. 14

Focal neurologic findings are commonly present6,14 and can signal increasing cerebral edema around
the abscess.4

Seizures are typically generalized.14

Papilledema indicates the disease process is well advanced and increased intracranial pressure is
present.14

Bulging fontanelles, irritability, and enlarging head circumference may be noted in infants.5

Causes
A wide variety of organisms can cause brain abscess, depending on the portal of entry, and up to one third may
be polymicrobial.3,6

Direct extension - Sinus, odontogenic, and otogenic sources are common.

o

Streptococcus species (aerobic and anaerobic) are most frequently isolated.

Other organisms include Bacteroides, Enterobacteriaceae, Pseudomonas, Fusobacterium,

Prevotella, Peptococcus, and Propionibacterium.

Hematogenous spread - Pathogens depend on predisposing source. Some common examples are
listed below.
o

Endocarditis -Streptococcus viridans, Staphylococcus aureus

Pulmonary infections -Streptococcus, Fusobacterium, Corynebacterium, and Peptococcus

species

Cardiac defects with right-to-left shunt -Streptococcus species

Intra-abdominal infections -Klebsiella species, E coli, other Enterobacteriaceae,

Streptococcus species, anaerobes

Urinary tract infections - Enterobacteriaceae, Pseudomonas species

Wound infection -S aureus

Penetrating head trauma, postoperative10

o

S aureus is most commonly isolated.

Enterobacteriaceae, other gram-negative bacilli, S epidermidis, Clostridium species,

anaerobes, and Pseudomonas species may also be found.

Propionibacterium acnes, an indolent gram-positive anaerobic organism, may cause delayed

postoperative brain abscess, even 10 years after an intracranial procedure. 17

Rarely, cases of brain abscess have been reported even after nonpenetrating traumatic intracranial
hemorrhage.18

Opportunistic infection is an increasing cause of brain abscess, as there are more patients with organ
transplant, HIV, and immunodeficiencies. Common organisms include Toxoplasma gondii and

Nocardia, Aspergillus, and Candida species.4,5,6 Cases of Nocardia are increasing even in
immunocompetent patients and have high mortality.2,4,19

Other predisposing risk factors include intravenous drug use, cardiac abnormalities (ie, prosthetic
valve, septal defect), cyanotic congenital heart disease (most common cause of multiple brain
abscesses in children), diabetes, chronic steroid use, alcoholism, and neoplasm. 2,9,14

Case reports of near drowning, foreign body aspiration, application of dental braces, tongue piercing,
and upper endoscopic procedures such as esophageal dilatation and variceal ligation have also been
associated with brain abscess.20,21,22,23,24,25

When there is no obvious source (up to 25% of cases), upper respiratory tract flora and anaerobes are
often isolated.2 Several sources have identified a patent foramen ovale by echocardiogram in these
cases and propose this as a possible mechanism for seeding oral flora to the brain. 26

Several cases of community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) causing

brain abscess have been reported recently, so this must be considered when initiating empiric therapy
in patients presenting with neurologic symptoms who also have risk factors for CA-MRSA. 27,28,29