Fever: present in 85% of children and up to 97% of adults (Lancet 338:406)
Neck stiffness (nuchal rigidity): 30% sensitivity, 68% specificity of adults.10,11,12 In children, it is a bit less helpful, but occurs in 78% of children by the age of 2.
Kernigs-with hip flexed, can not straighten knee passively
Brudzinskis-when you flex the neck, pt must flex hips (both of these have 5% Sensitivity, 95% specificity) Clin Infect Dis 35:46, 2002
Jolt Maneuver-A more promising examination involves the “jolt maneuver.” To perform this test, ask the patient to rapidly (2-3 times per second) shake his or her head from side to side. In one study, accentuation of the headache by this maneuver was 100% sensitive and 54% specific for meningitis; the studys authors claim that the test is the most useful adjunctive maneuver for evaluating headache in the presence of fever. (Headache. 1991 Mar;31(3))
(JAMA 1999, 282:175)
This unfortunately did not pan out on validation (The American Journal of Emergency Medicine Volume 31, Issue 11, November 2013, Pages 1601–1604)
The CBC should never be used to rule out meningitis; nearly one-third of patients with meningitis have a normal white count and differential
Meningicoccal-waterhouse friedrichson syndrome (bilat adrenal hemorrhage)
Adults-strep pneumo, neisseria, listeria
In the recent Canadian experience, CSF analyses of bacterial meningitis provide chilling data. Of 103 cases, only 56 had WBC counts greater than 1,000. 35% had counts from 100-1000, and a startling 10% had WBC counts under 100. All but one, however, had protein levels above 45, and 65% had levels of greater than 200.4 These cases represent primarily community acquired cases of meningitis in Alberta from 1985-1997. Of note, however, 43 out of a total of 103 patients had received previous antibiotics (Medicine. 79:6, 2000)
True CSF WBC=Measured-((CSF RBC x Blood WBC)/Blood RBC)
5 to 1000
0 to 45
15 to 45
5 to 2000
20 to 200
5 to 500
10 to 45
45 to 500
0 to 5
45 to 80
15 to 45
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Lactate in CSF
The CSF lactic acid readily differentiates bacterial (> 6 mmol/l), from partially treated (46 mmol/l), from viral meningitis (> 2 mmol/l),
5. Lannigan R, MacDonald MA, Marrie TJ, Haldane EV. Evaluation of cerebrospinal fluid lactic acid levels as an aid in differential diagnosis of bacterial and viral meningitis in adults. J Clin Microbiol. 1980;11:324-327. FREE FULL TEXT 56.
Lindquist L, Linne T, Hansson LO, et al. Value of cerebrospinal fluid analysis in the differential diagnosis of meningitis: a study of 710 patients with suspected central nervous system infection. Eur J Clin Microbiol Infect Dis. 1988;7:374-380. FULL TEXT | WEB OF SCIENCE | PUBMED 57.
Briem H. Comparison between cerebrospinal fluid concentrations of glucose, total protein, chloride, lactate, and total amino acids for the differential diagnosis of patients with meningitis. Scand J Infect Dis. 1983;15:277-284. WEB OF SCIENCE | PUBMED
Intensive Care Med. 1990;16(3):196-200. Cerebrospinal fluid lactate in 78 cases of adult meningitis.
Some would argue that differentiating between bacterial and viral by CSF parameters is a myth. Bacterial meningitis can exist within the range of viral parameters. (Can J Emerg Med 2003;5(5):348-9)
Glucose should be .6:1 CSF:Serum
Normal CSF pressure ranges from 5-20 cm CSF or <200 mm CSF when the patient is in the usual decubitus position. Measuring the pressure may occasionally be helpful, as CSF pressures may be significantly elevated in a variety of headache conditions. These include SAH, CVT, bacterial and cryptococcal meningitis, and pseudotumor cerebri.
1:750 WBC to RBC in traumatic tap (Roberts and Hedges)
For certain special situations, other choices or additions may be appropriate. In the neonate and the elderly (>60 y.o.), the addition of ampicillin is warranted due to increased rates of infection with Listeria monocytogenes, enterococci, and Streptococcus agalactiae.19 For immunocompromised patients, therapy should be expanded to cover for gram negative organisms, including Pseudomonas aeruginosa. Options for therapy in this situation include ampicillin and ceftazidime, or meropenem, with an aminoglycoside.19 Finally, in those with a recent history of neurosurgery or in the presence of a shunt, extra attention should be directed to Staphylococcus aureus with the addition of oxacillin/nafcillin or vancomycin.19 If the patient has an altered mental status, focal neurologic signs, or seizures, herpetic encephalitis should be considered. Furthermore, hemorrhagic encephalidites, most notably herpes encephalitis, may result in a significant number of RBCs in the cell count of an otherwise atraumatic lumbar puncture and should alert the EP to the presence of a possibly treatable viral etiology. In these cases, pending PCR results (where available) empiric therapy with acyclovir is warranted as this is the only treatment available to these patients The usual dosage is 10 mg/kg every 8 hours .24
Ceftriaxone 2g +
+- Amp 2g Q4
+- Acyclovir 10 mg/kg Q8
meropenem and cefotaxime are also good for s. penumo in the CNS
Dexamethasone is administered in a dose of 10 mg intravenously every six hours for four days and the regimen should be initiated before or with the first dose of antibiotics. Of note, vancomycin should not be used as the sole antibiotic in a patient with suspected pneumococcal meningitis who is receiving concomitant dexamethasone therapy, as there is the concern that a diminished CSF inflammatory response may substantially reduce vancomycin concentrations in cerebrospinal fluid and delay CSF sterilization. References: de Gans J, van de Beek D. Dexamethasone in adults with bacterial meningitis. N Engl J Med 2002;347:1549-1556.
Corticosteroids should be given as early as possible in all cases of ABM, using the published dose of dexamethasone, 10 mg every 6 hours in adults, or 0.4 to 0.6 mg/kg per d divided in 4 daily doses for children for 4 days. Ideally, dexamethasone should be administered before the antibiotics. (ACP Journal Club March/April 2004)
STEROIDS IN ADULTS WITH ACUTE BACTERIAL MENINGITIS: A SYSTEMATIC REVIEW Lancet Infect Dis 4:139, March 2004 CONCLUSIONS: The authors feel that these findings support the use of adjunctive steroid treatment in adults with acute bacterial meningitis. They recommend a four-day course of IV dexamethasone (10mg every six hours), begun before or with the first dose of antibiotics, except in patients who are immunocompromised, are in septic shock, have already been treated with parenteral antibiotics, or have post-neurosurgical meningitis. 32 references
Negative steroid study (NEJM 2007;357:2441) Mildly positive steroid study even after abx (NEJM 2007;357:2431)
Individual Pt Meta-Analysis shows no benefit (Lancet Neurol 2010;9(3):254)
Guidelines for Bacterial Meningitis (CID 2004;39)
10% of bacterial meningitis will present with lymphocytic predominance
CSF lactate for post-op patients
meningitis gram negative diplococci=neisseria
CHEMOPROPHYLAXIS OF MENINGOCOCCAL AND HiB MENINGITIS
TO WHOM? Patient and close contacts*
ALTERNATIVES Rifampin (orally)
ADULTS 600 mg b.i.d. for 2 days
Meningococcal disease 10 mg/kg b.i.d. for 2 days
Hib disease 20 mg/kg once daily for 4 days
ADULTS 250 mg, 1 single dose
CHILDREN 125 mg, 1 single dose
Ofloxacin400 mg, 1 single dose orally (adults)
Ciprofloxacin500 mg, 1 single dose orally (adults)
Azithromycin500 mg, 1 single dose orally (adults, meningococcal disease)
4 doses of Rifampin if exposed to n. meningitides
Chemoprophylaxis Against Meningococcal Disease – Who Needs It? When an Emergency Physician identifies a case of meningococcal disease, the patient’s close contacts must be prescribed an effective antimicrobial agent to eradicate potential colonization by N. meningitidis. Frequently, an overreaction ensues regarding who actually needs to be treated. The definition of “close contact” is not precise, but it is intended to include persons who have had prolonged (> 8 hours) contact while in close proximity (3 ft is the general limit for large-droplet spread) to the patient or who have been directly exposed to the patient’s oral secretions (e.g., through prolonged face-to-face contact, mouth-to-mouth resuscitation, kissing, or management of an endotracheal tube) within 1 week before the onset of the patient’s symptoms until 24 hours after appropriate antimicrobial therapy has been initiated. Such persons typically include members of the household and roommates, persons at a child-care center, and others who have had prolonged exposure to the infected patient (e.g., travelers on an airplane seated next to the patient for more than 8 hours) (1,2). Classmates and coworkers are not included unless they meet the criteria for close contact. Close contacts who have previously received meningococcal vaccination should still be given chemoprophylaxis, because the vaccines do not confer 100% protection and immunity wanes with time. Ideally, chemoprophylaxis should be started within 24 hours after the index case has been identified, although diminishing levels of benefit may still be realized even with delays of up to 2 weeks (1,3).References: (1) Gardner P. Prevention of Meningococcal Disease NEJM 2006; 355:1466-1473. (2) Guidelines for the management of airline passengers exposed to meningococcal disease. Atlanta:Centers for Disease Control and Prevention, 2000 (http://www.cdc.gov). (3) Prevention and control of meningococcal disease: recommendations of the Advisory Committee on Immunization Practices (ACIP) MMWR Recomm Rep 2005;54:1-21.
Review Article (NEJM 2006;354(1):44)
In another study, at least 1 of 4 key elements (headache, fever, neck stiffness, and alterations in mental status) was present in 99% of patients, suggesting that aspects of history and physical examination can be used to heighten suspicion of meningitis even if they cannot alone rule out the diagnosis. Although increased intracranial pressure may result in brain herniation following lumbar puncture, several studies have shown no clinical changes in patients who had lumbar puncture to diagnose meningitis. In the opinion of the authors, it is reasonable to proceed with lumbar puncture without a computed tomographic (CT) scan if the patient does not have any of the following: new-onset seizures, an immunocompromised state, signs that are suspicious for space-occupying lesions (papilloedema or focal neurologic signs excluding cranial nerve palsy), or moderate-to-severe impairment of consciousness. Lancet Infect Dis. 2007;7:191-200.
Initial Tap-negative Meningitis
It is a popular misconception that a normal CSF excludes the diagnosis of bacterial meningitis. However, our case, and others reported in the literature, demonstrate that an initial normal CSF might later yield a positive organism on culture. A normal CSF is defined as less than 5 white cells per cubic millimetre, with no more than 1 polymorphonuclear cells, glucose level greater than 40% of the serum glucose concentration, less than 45 mg/dL of protein and a negative Gram stain. In a study by Polk and Steele of 261 patients from a large paediatric hospital over a 6 year period, 7 (2.7%) had a positive CSF culture despite initially normal CSF parameters.2 This report also found that the spectrum of the patients’ ages and the recovered pathogen was rather varied. Another study of 82 patients with documented meningococcal meningitis reported that 8 (9.7%) initially had normal CSF results.3 None had received previous antibiotic treatment. Other authors have reported that meningitis with an initially normal CSF accounts for 0.5% to 12% of all cases of bacterial meningitis.3 The causative organisms are usually common meningeal pathogens (N. meningitidis, H. influenzae and S. pneumoniae),3 although other organisms causing a similar clinical picture have been described (P. mirabilis, group B Streptoccus).2,4
1. Van de Beek D, De Gans J, Spanjaard L, Weisfelt M, Reitsma JB, Vermeulen M. Clinical features and prognostic factors in adults with bacterial meningitis. N Engl. J. Med. 2004; 351: 184959. CrossRef, Medline, ISI 2. Polk DB, Steele RW. Bacterial meningitis presenting with normal cerebrospinal fluid. Pediatr. Infect. Dis. J. 1987; 6: 104042. 3. Coll M, Uriz M, Pineda V et al. Meningococcal meningitis with normal cerebrospinal fluid. J. Infect. 1994; 29: 28994. CrossRef, Medline, ISI, CSA 4. Onorato IM, Wormser GP, Nicholas P. Normal CSF in bacterial meningitis. JAMA 1980; 244: 146971. CrossRef, Medline, ISI
(from Emerg Med Austral 2007;Dec)
Negative cell count, Positive Cultures???
The Journal of Emergency Medicine Volume 37, Issue 3, October 2009, Pages 251-256
Follow-up may be unnecessary in ED patients with positive bacterial CSF cultures who were discharged from the ED, if their initial lumbar punctures were normal.
S suis is a Gram-positive, facultatively anaerobic coccus that has been implicated as the cause of a wide range of clinical disease syndromes in swine and other domestic animals. S suis has also been implicated in human disease, especially among abattoir workers and swine and pork handlers. S suis infection is found in all pig-raising countries. Worldwide, hospitals in Hong Kong, The Netherlands, Greece, Spain, Japan (S suis type 2), Croatia (S suis type 1), Taiwan, Singapore, United Kingdom, Austria, Belgium, Canada, Italy, New Zealand, Sweden and Latin America have reported cases. Cases in Germany, The Netherlands and France have been acquired from wild boar. Occupational seropositivity has been documented in New Zealand and The Netherlands. Virtually all patients have been farmers and butchers, of whom 80% were men. Most had been involved in butchering sick pigs or selling the pork.1 There has been no evidence of human-to-human transmission.2
Reported symptoms include high fever, malaise, nausea and vomiting, followed by meningitis, pneumonia, subcutaneous haemorrhage, polyarthritis, toxic shock and coma in severe cases. The time from pig exposure to the onset of symptoms is short and the disease progresses rapidly. In humans, 80% of all cases are due to meningitis, and it is found to be one of the third commonest causes of meningitis in Hong Kong.3 Toxic shock syndrome with haemorrhagic manifestations rarely develops.
The organism is found to be sensitive to penicillin and cephalosporin. Complications resulting from S suis meningitis include neurological sequelae such as ataxia, disturbance of gait and bilateral hearing impairment.2
The WHO released an epidemic and pandemic alert, after an outbreak of S suis infection in China during the summer of 2005, with 206 cases reported and a case fatality rate of 18%. There was a suggestion that the outbreak was associated with a new strain of the bacterium4 more able to adapt to humans.
Further occurrences of S suis illness can be prevented by increasing awareness of the disease with the education of farmers, pig and pork handlers. The Health Protection Agency recognises this infection as an occupational hazard, but not as a notifiable disease. Due to the virulent nature of the infection, people at risk should be educated about the warning symptoms, signs and advised to seek medical help early. Vaccines with uncertain efficacy have been used in swine to prevent virulent infection; however, vaccines for humans at risk are yet to be developed.
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Can be due to bacteria, fungi, or protozoa. Usually from direct extension, such as sinusitis, but also may be from large bacteremia.
chart from http://www.ferne.org
Excellent Review (Clin Infect Dis 25: 763-781; 1997)
Patients may present without fever, without white count. LP will be negative and may be dangerous.
Frontal lobe can be totally asymptomatic
Usually anaerobic, strep, enterobacteriaceae, and staph are the most common aerobes.
Ceftriaxone and Flagyl provides good coverage
Pseudomonas pseudomallei, which produces discrete abscesses like this and which is endemic in Southeast Asia. They often present as focal seizures.
Hereditary Hemorrhagic Telangiectasia (HHT) or Osler-Weber-Rendu: autosomal dominant. Telangiectasias and AVMs in lungs, liver GI, and brain. Triad of telangiectasias, recurrent epistaxis, and family history. Pulmonary AVMs allow for paradoxical embolisms. Brain abscess from septic emboli
Give ceftriaxone and flagyl
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Viral encephalitis is usually called by arbovirus or a herpes virus
Herpes Virus Encephalitis is caused by HSV-1, Varicella, Epstein-Barr, or CMV.
With a sensitivity and specificity > than 95%, PCR testing of CSF for herpes viruses is considered the criterion standard for diagnosing herpes virus meningitis/encephalitis (Mayo Clin Proc, 12/107, pg. 1562).emedhome
If patients have received brain irradiation, they can have HSV encephalitis with a normal cell count and probably should be empirically treated (Crit Care Med 2012;40:1304)
Acute Disseminated Encephalomyelitis (ADEM) is an autoimmune disorder that occurs several weeks after a viral illness. It is probably the cause of up to 1/3 of viral encephalitis. Steroids are usually given, if they fail IVIG or plasmapheresis.
The most common arboviruses are St. Louis and West Nile.
Since disseminated by arthopod vector, predominate in warm summer months
CTs are negative, MRI will show changes in HSV
Virus testing of the CSF can be done with PCR.
Acyclovir improves HSV encephalitis, probably not helpful in West Nile.
A disease of mosquitoes and birds. Human to human transmission has only been documented with blood transfusions. The transfusions and mosquitoes are the only known vectors for the disease.
Incubation is 3 to 14 days
Onset of the infection is West Nile Fever: syndrome of fever, myalgias, headache, and GI symptoms. Maculopapular rashes are occasionally noted as well.
Most people will produce IgM and clear the virus without further progression.
In some, the virus will cross the BBB and a meningoencephalitis will develop.
The damage is most consistently to the brainstem.
It will present with fever, headache, and possibly, decreased DTR, muscular weakness sometimes with flaccid paralysis, and respiratory compromise.
CSF will usually demonstrate pleocytosis, lymphocyte predominance, increased protein, and normal glucose.
An elisa for IgM is available.
temporal or parietal abnormalities on CT or MRI.
Untreated mortality rate of ~80%
CSF shoes pleocytosis with polys or lymphocytes
RBCs are usually present
Need CSF PCR
Most cases are from HSV-1 but HSV-2 is also seen
consider syphyllis in the diagnosis
The human herpesvirus (HHV) family, also known as herpes simplex virus (HSV), includes two clinically important strains. Herpes simplex virus type 1 (HSV-1) typically causes oral lesions, while herpes simplex virus type 2 (HSV-2) usually causes genital lesions. Both strains also may be associated with encephalitis, commonly called herpes simplex encephalitis (HSE). HSV-1 is more commonly implicated in adult encephalitis, while HSV-2 more typically causes newborn encephalitis through spread from the maternal genital tract [1, 2 and 3].
Herpes simplex encephalitis is the most common cause of sporadic viral encephalitis, accounting for approximately two cases per million persons per year in the United States [1 and 4]. The disease affects men and women equally and has no seasonal variability. Approximately one-third of cases develop in patients under 20 years of age and one-half in patients over 50 years [1 and 2].
Symptoms of HSE are variable. Patients often will have a prodrome of malaise, fever, headache, and nausea. This prodrome is followed by the onset of either acute or subacute encephalopathy, typically manifested by lethargy, confusion, delirium, personality change, or even coma. Focal neurological deficits are common, with seizure, ataxia, hemiparesis, and dysphasia all typical findings. Physical examination of patients with HSE is also variable. The neurological examination may be completely normal or can reveal focal or generalized deficits [1, 2, 4 and 5]. Additionally, the absence of nuchal rigidity is suggestive of encephalitis as opposed to meningitis .
In suspected cases of HSE, the work-up must be initiated rapidly, although treatment should not be delayed while making the diagnosis. Neurodiagnostic tests that can support a presumptive diagnosis of HSE include brain CT or MRI scanning, CSF analysis, EEG, and historically, brain biopsy.
Imaging studies are often helpful in making the diagnosis, but may be more useful in ruling out other pathology. The CT scan of the head may show low-density lesions, especially in the temporal lobes. However, these lesions are only present in two-thirds of cases and may not appear until 3 to 4 days after symptom onset . The MRI is more accurate than a CT scan and is now considered the imaging study of choice in suspected cases of HSE. Pathologic changes in the infero-medial portion of the temporal lobes are most commonly displayed on T2 hyper-intensity images and are highly suggestive of HSE [2 and 6].
Additional investigation should include a lumbar puncture, once a space-occupying lesion has been ruled out by imaging studies. Common lumbar puncture results include a mononuclear pleocytosis with mildly elevated protein and normal glucose [1 and 2]. Also, because of the hemorrhagic nature of the infectious process, red blood cells and xanthochromia are commonly seen, but are not diagnostic. A small percentage of patients will have completely normal CSF.
The HSV virus only rarely can be cultured from CSF. As a result, PCR analysis of the CSF is the preferred diagnostic test in HSE as it is highly sensitive and specific in making the diagnosis and will remain positive up to 5 days after the initiation of antiviral therapy [2, 3 and 7].
Electroencephalography (EEG) can be of value in confirming the diagnosis of HSE. Characteristic periodic high-voltage spike wave activity emanating from the temporal lobes and slow wave complexes are highly suggestive of HSE. These findings are present in four-fifths of biopsy-proven cases of HSE, and have a sensitivity of 84% and specificity of 33% [1 and 2].
Historically, brain biopsy was considered the only definitive means of diagnosing HSE . However, since the advent of PCR analysis of CSF, the role of biopsy has markedly diminished.
Standard pharmacotherapy for HSE is intravenous Acyclovir at a dose of 10 mg/kg every 8 h, with dose adjustment for renal insufficiency. Acyclovir has completely supplanted Vidarabine, which is less effective and more toxic . Intravenous Acyclovir should be initiated as soon as the diagnosis of HSE is suspected rather than delayed until the diagnosis is confirmed; delayed initiation of Acyclovir treatment for more than 2 days after hospital admission is associated with poor outcomes .
HSE is progressive and often is fatal in 7 to 14 days if not treated. A landmark study by Whitley et al. in 1977 reported a 70% mortality rate in untreated patients and severe neurological deficits in most survivors [1 and 4]. Even in treated cases of HSE, the mortality rate is still high, while complications and neurological sequelae are also common .
Herpes simplex virus infection of the brain is the only viral CNS infection for which therapy has been proven useful in controlled trials. Successful therapy depends on considering the possibility of the disease and the early institution of antiviral therapy. The presence of CSF pleocytosis and elevated protein in a patient with encephalopathy in the absence of identifiable pathogens should be considered due to HSV until proven otherwise. (JEM 2004, 26:1)Back to top
This is an autoimmune disorder with production of auto-antibodies targeting the NR subunit of the NMDA receptor. The NMDA receptor is scattered throughout the brain and is involved in synaptic transmission. This disease was first described in 2005 in four females with ovarian teratomas. This is not the Ecstasy NMDA that we love. This is a completely different entity. Lancet published a case series with 577 patients. Titulaer MJ et al. Treatment and prognostic factors for long- term outcome in patients with anti-NMDA receptor encephalitis: an observational cohort study. Lancet Neurol. 2013 Feb;12(2):157-65. PMID: 23290630. u Teratomas are frequently involved. These are the weird tumors with teeth and eyeballs. They also have neuronal tis- sue with NMDA receptors. After an inciting event, the immune system recognizes the neuronal tissue as foreign and attacks it. This leads to a cross-reaction between the antibodies and the NMDA receptors in the brain. u Although this was initially thought to be a paraneoplas- tic process, it is not. u This is a disease of the young. The mean age is 21 years. In the study, the ages ranged from 8 months to 85 years. 37% are under the age of 18 years. u 38% have a paraneoplastic phenomenon. Of these, the majority occurs in women (97%). 94% are due to ovarian teratomas. It is more common in patients of African American, Asian American and Pacific Islander descent due to their higher incidence of ovarian teratomas. u Some estimate that this represents 4% of cases of en- cephalitis. It may be responsible for up to 20% of cases of encephalitis in patients under the age of 30 years. The Cali- fornia Encephalitis Project found that anti-NMDA receptor encephalitis has a higher incidence than all the common individual encephalopathies. It is more common than HSV encephalitis in young patients. u The treatment of choice is IVIG and steroids. Patients are usually given 5 days of high dose methylprednisolone (about 1g a day). u If you have a patient who is acting weird, psychotic, altered, having seizures, get in touch with your neurology and critical care colleagues to determine if the patient could benefi from IVIG and steroids. u There are four described phases. The first phase is the prodromal phase. This is like a viral illness with headache, fever, and upper respiratory infection symptoms. This occurs in 60-80%. The next phase often occurs within a few days to several weeks. This is the psychotic phase characterized by memory changes, like anterograde amnesia, and behavioral changes, like paranoia, delusions, and hallucinations. This can occur in 70-80%. Seizures occur in 75% of patients. The third phase is the unresponsive phase characterized by catatonia, choreiform movements, and orofacial dyskinesia. It is estimated that up to 85% have lip-smacking. The final phase is a hyperkinetic phase with autonomic instability. 70-90% will have fluctuations in heart rate, blood pressure, and salivary function.
u This can be a difficult diagnosis to make. If you have a patient with altered mental status, you need to LP them, even if they don’t have a fever. 90% of these patients will have a lymphocytic pleocytosis in their CSF. They might have increased protein. Glucose should be normal. 60% will have oligoclonal bands. The EEG will show seizures. MRIs won’t help you much; only about 40% are abnormal.
• The CSF should be sent for auto-antibodies or anti-NMDA receptor antibodies. This is an immunofluorescent assay looking for antibodies to the NR1 receptor. These are present in the serum as well, but to a lesser degree.
u Early treatment has been found to be a predictor of good outcome. The other predictor of good outcome is a paraneoplastic cause; once you remove the teratoma, they are much less likely to have recurrence. Patients, especially young women, should have an age-appropriate malignancy work-up. 81% will have a good outcome in 3 months, but only about 15% will get better in the first month. Early intervention makes a difference.
u Laboratory testing can take 10 days to obtain a result. The patient may be treated empirically.
u Consider this disease in young patients with altered mental status, seizures, and movement disorders. Neuroleptic malignant syndrome mimics this.
u Most are unaware of these syndromes. You can make a difference by making this diagnosis.
u A book describing this condition was published by a writer at the NY times. Brain on Fire: My Month of Madness by Susannah Cahalan.
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Localized Neuro Findings
Hemiparesis may occur through a wide variety of mechanisms, including cortical vein or sagittal sinus thrombosis, cerebral artery spasm, subdural empyema, hydrocephalus, cerebral infarction, abscess, or edema (Mayo Clin Proc, Vol. 80, pg. 1070).
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(from Crit Care Reviews)
ICP guided therapy was associated with
- a lower mortality at 2 months
- 10% versus 30%; relative risk reduction 68%; p<0.05
- improved recovery (Glasgow outcome score and hearing)
- 54% versus 32%; relative risk reduction 40%; p<0.05