Viral meningitis
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2] Ahmed Elsaiey, MBBCH [3]
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Synonyms and keywords: Aseptic meningitis, Non-infectious meningitis, Non-pyogenic meningitis, Enteroviral meningitis
Overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]
Overview
Viral meningitis is a condition in which the layers lining the brain, or meninges, become inflamed due to a viral infection. Meningitis is diagnosed on a history of characteristic symptoms and certain examination findings (e.g. Kernig’s sign). Investigations should show an increase in the number of leukocytes present in the cerebrospinal fluid (CSF), obtained via lumbar puncture.
Historical Perspective
Meningitis was first discovered by Hippocrates. Wallgren described aseptic meningitis in 1924 and defined it as a disease with acute onset that had typical systematic symptoms of meningeal involvement, in association with a cerebrospinal fluid (CSF) typical of meningitis (typically with a mononuclear cell predominance). Additionally, there was absence of bacteria on stain and culture and there was no identifiable parameningeal infection.
Classification
There is no specific classification to the viral meningitis. However, it may be classified based on the age into child and adult viral meningitis. It may be also according to the causative virus like enterovirus, arbovirus, mumps and herpes simplex viruses.
Pathophysiology
Viral meningitis pathophysiology may differ from virus to another and depends on many factors like age, immune status and gene expression. Invasion into the meninges by a pathogen can set up a local inflammatory response. The clinical signs are due to this meningeal irritation. Kernig’s sign is due to pain produced by stretching of the inflamed meninges.
Causes
Viral meningitis is caused by many viruses. The most important and the most common virus group that causes meningitis is Enteroviruses group. There are other viruses cause meningitis as arbovirus and herpes simplex virus groups but not common as the enteroviruses.[1][2][3]
Differential diagnosis
The differential diagnosis of viral meningitis includes two step approach. First is differentiating viral meningitis from other diseases which have similar clinical presentation as viral meningitis such as encephalitis, brain abscess, subarachnoid hemorrhage, and brain tumour. Second step involves CSF examination and differentiating viral meningitis from bacterial, fungal and other causes of meningitis
Epidemiology and demographics
Viral meningitis affect around 26,000 to 42,000 individual annualy with incidence 11 per 100,000 population. There is no gender or racial predilection.
Risk Factors
Viral meningitis risk factors rely particularly on the exposure to the infection itself and the route of transmission like respiratory droplet and feco-oral transmission. However, there are people at risk to be infected by the disease as children less than 5 years and immunocompromised patients.[4]
Natural History, Complications and Prognosis
Viral meningitis is a self resolved disease if left untreated. It takes around 10 days to be resolved. Seizures and loss of consciousness are the most important complications that may appear in the infants younger than 3 months. It has an excellent prognosis.
Diagnosis
History and symptoms
Viral meningitis symptoms are varied, depending on the causative organism. The symptoms of viral meningitis usually last from 7 to 10 days, and people with normal immune systems usually recover completely. A rash may be present, which could suggest a particular virus e.g. varicella zoster. However, a non-blanching purpuric rash is not associated with meningitis and suggests systemic bacterial infection. The more common symptoms of meningitis are fever, severe headache, stiff neck, bright lights hurting the eyes, drowsiness or confusion, and nausea and vomiting. In babies, the symptoms are more difficult to identify. They may include fever, irritability, difficulty in awakening the baby, or the baby refuses to eat. The symptoms of meningitis may not be the same for every person.
Physical examination
Viral meningitis patients appear lethargic and may be not well oriented. They also appears feverish grading (40°C/104°F). The signs may differ according to the patient age and the virus causing the disease as well. Different signs can be noticed like photophobia, phonophobia, nuchal rigidity, altered mental status, and skin rash.
Laboratory findings
Viral meningitis lab tests include non specific blood tests like the CBC, blood culture, PT and PTT tests. Other tests include some tissues swabbing like the throat and nose swab to detect the viruses. PCR is also recommended for virus detection. CSF studies is the most important specific diagnostic test for the viral meningitis and it also differs between the various types of meningitis.
CT scan
Viral meningitis diagnosis depends on mainly the CSF studies. CT scan is required for imaging before applying the lumbar puncture to see if there is any contraindication for the procedure. However, CT scan may be performed to exclude other brain diseases that can be misinterpreted with the viral meningitis.[5]
MRI
Viral meningitis diagnosis depends on mainly the CSF studies.However, MRI scan may be performed to exclude other brain diseases that can be misinterpreted with the viral meningitis.
Ultrasound
There are no ultrasound findings associated with viral meningitis.
Xray
There are no x-ray findings associated with viral meningitis.
Other imaging findings
There is no other imaging findings to diagnose the viral meningitis.
Other diagnostic studies
There is no other diagnostic studies for the viral meningitis.
Treatment
Medical therapy
Viral meningitis has no specific treatment as most of the patients recover within 7-10 days. General supportive measures are recommended to manage the cases and prevent proceeding to serious conditions like the brain edema. These measures include: analgesics for the pain, acetaminophen for the fever and electrolytes management However, antiviral medical therapy can be provided for the patients caused with specific viruses like the enteroviruses or the influenza. In severe cases, the patients will need to be hospitalized.
Surgery
Surgical intervention has no role in the management of viral meningitis.
Prevention
Primary prevention of viral meningitis depends mainly on the self hygiene and some measures that should be considered like: washing hands regularly, avoid touching face, avoid close contact with suspected individuals, and staying home when feeling sick. There are no vaccines against the enteroviruses but other viruses like influenza should be vaccinated to prevent the development of the disease. There is no secondary prevention for viral meningitis.
References
- ↑ Logan SA, MacMahon E (2008). “Viral meningitis”. BMJ. 336 (7634): 36–40. doi:10.1136/bmj.39409.673657.AE. PMC 2174764. PMID 18174598.
- ↑ Rotbart HA (2000). “Viral meningitis”. Semin Neurol. 20 (3): 277–92. doi:10.1055/s-2000-9427. PMID 11051293.
- ↑ Yi EJ, Shin YJ, Kim JH, Kim TG, Chang SY (2017). “Enterovirus 71 infection and vaccines”. Clin Exp Vaccine Res. 6 (1): 4–14. doi:10.7774/cevr.2017.6.1.4. PMC 5292356. PMID 28168168.
- ↑ CDC https://www.cdc.gov/meningitis/viral.html Accessed on April 10, 2017
- ↑ Nagra I, Wee B, Short J, Banerjee AK (2011). “The role of cranial CT in the investigation of meningitis”. JRSM Short Rep. 2 (3): 20. doi:10.1258/shorts.2011.010113. PMC 3086327. PMID 21541088.
Historical Perspective
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]Ahmed Elsaiey, MBBCH [3]
Overview
Meningitis was first discovered by Hippocrates. Wallgren described aseptic meningitis in 1924 and defined it as a disease with acute onset that has typical systematic symptoms of meningeal involvement, in association with a cerebrospinal fluid (CSF) typical of meningitis (typically with a mononuclear cell predominance). Additionally, there was absence of bacteria on stain and culture and there was no identifiable parameningeal infection.[1]
Historical perspective
- Meningitis was described first by the hippocrates, but it was first accurately identified by the Swiss Vieusseux (a scientific-literary association) during an outbreak in Geneva, Switzerland in 1805.[2]
- In 1661, Thomas Willis first described the inflammation of meninges and an epidemic of meningitis.
- In 1891, Heinrich Quincke provided an early analysis of CSF by introducing a new technique of lumbar puncture.
- In early 19th century, detailed profile of CSF analysis in meningitis was explained by William Mestrezat, and H. Houston Merritt.
- Wallgren first described aseptic meningitis was in 1924.
References
- ↑ GARD S (1954). “The etiology of acute aseptic meningitis (Wallgren)”. Acta Paediatr Suppl. 43 (100): 54–64. PMID 13228013.
- ↑ Tyler KL (2010). “Chapter 28: a history of bacterial meningitis”. Handb Clin Neurol. 95: 417–33. doi:10.1016/S0072-9752(08)02128-3. PMID 19892131.
Classification
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]
Overveiew
There is no specific classification to the viral meningitis. However, it may be classified based on the age into child and adult viral meningitis. It may be also according to the causative virus like enterovirus, arbovirus, mumps and herpes simplex viruses.
Classification
There is no specific classification to the viral meningitis. However, it can be classified according to the age and the causative virus.
- Age:
- Infantile viral meningitis
- Adult viral meningitis
- Causative viruses:
- Enteroviruses
- Arboviruses
- Mumps
- Herpes simplex viruses
Reference
Pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2],Ahmed Elsaiey, MBBCH [3]
Overview
Viral meningitis pathophysiology differs from virus to another and depends on many factors like age, immune status and gene expression. Invasion into the meninges by a pathogen can set up a local inflammatory response. The clinical signs are due to this meningeal irritation – for example, Kernig’s sign is due to pain produced by stretching of the inflamed meninges.
Pathogenesis
- The causative viral agents can reach the nervous system via the blood or the nerves themselves. There is a difference in both pathways pathogenesis. Viral spreading through the blood (viremia) is more common in viral meningitis pathogenesis. The viruses enter to the pulmonary and intestinal mucosa at which they spread into the blood to reach the lymph nodes where viral replication takes place and this is called primary viremia. At this point, the host cells try to prevent further replication from happening and if they fail to stop the replication, secondary viremia will take place and the viruses can spread to the nervous system causing many clinical manifestations.[1]
- Enteroviruses:
- They include coxsackievirus A&B, echovirus, hepatitis A, and poliovirus.
- Infection can be started in the nasal mucosa and after that it can be ingested in the stomach. It attaches to the enterocytes then the viruses reach the peyer’s patches of the lamina propria where the replication takes place.
- The replication which occurs at this site causes viremia to further organs like the lung, brain and liver at which another replication takes place at these organs causing more viremia. Infection of the nervous system can occur via this viremia which is responsible for the clinical manifestaions of the disease.
- Arboviruses:
- Common arvboviruses in the United States[2]:
- St. louis encephalitis virus (Flavivirus)
- Western equine encephalitis virus (Alphavirus)
- Colorado tick fever virus (Coltivirus)
- They commonly cause encephalitis. However, they are responsible for causing viral meningitis.
- Pathogenesis is similar to the enteroviruses pathogenesis. The difference between them is in the start process of the infection. The infection starts by the arthropod bite to the skin then virus replication takes place in the lymph nodes then viremia occurs in the distant organs and finally the virus reaches the brain.
- Common arvboviruses in the United States[2]:
- Mumps:
- Infection occurs through respiratory droplet that infects first the parotid gland causing parotitis.
- After the infection, viremia takes place and the virus reaches the brain causing meningitis.
- Human herpes viruses:[3]
- They include: Herpes simplex virus 1, Herpes simplex virus 2, human herpes virus 1, Cytomegalovirus, epstein barr virus and human herpes virus 8.
- Primary infection by the herpes viruses is like the other viral infections by invasion through the respiratory and gastric mucosa and the replication followed by the viremia till reaching the brain causing meningitis.
- Latent infection may occur when the virus is stimulated again by tissue damage or exposure to ultraviolet light.
Transmission
Infectious transmission is different among the viruses causing viral meningitis:
- Enteroviruses: Feco-oral transmission and may be transmitted by the respiratory droplet
- Herpes simplex virus: Inter-human transmission
- Arboviruses, such as West nile virus : Transmitted through mosquitoes bite
- Mumps: Transmitted via the blood
- Influenza: Postinfections – airborne transmission
- Lymphocytic choriomeningitis virus: Transmitted from the rodents
Genetics
There is no genetic inheritance correlated with the viral meningitis.
Microscopic pathology
Microscopic pathological findings in viral meningitis may include the following:
- Pleocytosis (10-1000 cells/µl)
- Polymorphous population of lymphocytes
- Activated lymphocytes
- Plasma cells may be binuclear or multinuclear
- Activated monocytes
References
- ↑ Rotbart HA (2000). “Viral meningitis”. Semin Neurol. 20 (3): 277–92. doi:10.1055/s-2000-9427. PMID 11051293.
- ↑ Calisher CH (1994). “Medically important arboviruses of the United States and Canada”. Clin Microbiol Rev. 7 (1): 89–116. PMC 358307. PMID 8118792.
- ↑ Koeller KK, Shih RY (2017). “Viral and Prion Infections of the Central Nervous System: Radiologic-Pathologic Correlation: From the Radiologic Pathology Archives”. Radiographics. 37 (1): 199–233. doi:10.1148/rg.2017160149. PMID 28076019.
Causes
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]
Overview
Viral meningitis is caused by many viruses. The most important and the most common virus group that causes meningitis is Enteroviruses group. There are other viruses cause meningitis as Arbovirus and herpes simplex virus groups but not common as the enteroviruses.[1][2][3]
Causes
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References
- ↑ Logan SA, MacMahon E (2008). “Viral meningitis”. BMJ. 336 (7634): 36–40. doi:10.1136/bmj.39409.673657.AE. PMC 2174764. PMID 18174598.
- ↑ Rotbart HA (2000). “Viral meningitis”. Semin Neurol. 20 (3): 277–92. doi:10.1055/s-2000-9427. PMID 11051293.
- ↑ Yi EJ, Shin YJ, Kim JH, Kim TG, Chang SY (2017). “Enterovirus 71 infection and vaccines”. Clin Exp Vaccine Res. 6 (1): 4–14. doi:10.7774/cevr.2017.6.1.4. PMC 5292356. PMID 28168168.
Differentiating Viral Meningitis from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]
Overview
The differential diagnosis of viral meningitis includes two step approach. First is differentiating viral meningitis from other diseases which have similar clinical presentation as viral meningitis such as encephalitis, brain abscess, subarachnoid hemorrage, and brain tumour. Second step involves CSF examination and differentiating viral meningitis from bacterial, fungal and other causes of meningitis
Differential diagnosis
Differentiating viral meningitis from other diseases
Viral meningitis may mimick other diseases in terms of clinical signs and symptoms. It is important to differentiate viral meningitis from other diseases with similar presentation. Once the diagnsis of meningitis is confirmed, the next step may be to differentiate different types of meningitis on the basis of CSF examnination:[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16]
Differentiating viral meningitis from other diseases
| Diseases | Diagnostic tests | Physical Examination | Symptoms | Past medical history | Other Findings | |||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Na+, K+, Ca2+ | CT /MRI | CSF Findings | Gold standard test | Neck stiffness | Motor or Sensory deficit | Papilledema | Bulging fontanelle | Cranial nerves | Headache | Fever | Altered mental status | |||
| Brain tumour[2][3] | + | Cancer cells[4] | MRI | + | + | + | + | + | + | Cachexia, gradual progression of symptoms | ||||
| Delerium Tremens | + | Clinical diagnosis | + | + | + | + | + | + | Alcohal intake, sudden witdrawl or reduction in consumption | Tachycardia, diaphoresis, hypertension, tremors, mydriasis, positional nystagmus, tachypnea | ||||
| Subarachnoid hemorrhage[17] | + | Xanthochromia[5] | CT scan without contrast[7][8] | + | + | + | + | + | + | + | + | Trauma/fall | Confusion, dizziness, nausea, vomiting | |
| Stroke | + | Normal | CT scan without contrast | + | + | + | + | + | TIAs, hypertension, diabetes mellitus | Speech difficulty, gait abnormality | ||||
| Neurosyphilis[18][19] | + | ↑ Leukocytes and protein | CSF VDRL-specifc
CSF FTA-Ab -sensitive[20] |
+ | + | + | + | + | + | Unprotected sexual intercourse, STIs | Blindness, confusion, depression,
Abnormal gait | |||
| Viral encephalitis | + | Increased RBCS or xanthochromia, mononuclear lymphocytosis, high protein content, normal glucose | Clinical assesment | + | + | + | + | + | + | + | Tick bite/mosquito bite/ viral prodome for several days | Extreme lethargy, rash hepatosplenomegaly, lymphadenopathy, behavioral changes | ||
| Herpes simplex encephalitis | + | Clinical assesment | + | + | + | + | + | History of hypertension | Delirium, cortical blindness, cerebral edema, seizure | |||||
| Wernicke’s encephalopathy | Normal | + | + | + | History of alcohal abuse | Ophthalmoplegia, confusion | ||||||||
| CNS abscess | + | ↑ leukocytes >100,000/ul, ↓ glucose and ↑ protien, ↑ red blood cells, lactic acid >500mg | Contrast enhanced MRI is more sensitive and specific,
Histopathological examination of brain tissue |
+ | + | + | + | + | + | + | History of drug abuse, endocarditis, ↓ immune status | High grade fever, fatigue,nausea, vomiting | ||
| Drug toxicity | + | + | Lithium, Sedatives, phenytoin, carbamazepine | |||||||||||
| Conversion disorder | Diagnosis of exclusion | + | + | + | + | + | Tremors, blindness, difficulty swallowing | |||||||
| Electrolyte disturbance | ↓ or ↑ | Depends on the cause | + | + | Confusion, seizures | |||||||||
| Febrile seizures | Not performed in first simple febrile seizures | Clinical diagnosis and EEG | + | + | + | + | Family history of febrile seizures, viral illness or gastroenteritis | Age > 1 month, | ||||||
| Subdural empyema | + | Clinical assesment and MRI | + | + | + | + | + | + | History of relapses and remissions | Blurry vision, urinary incontinence, fatigue | ||||
| Hypoglycemia | ↓ or ↑ | Serum blood glucose | + | + | + | History of diabetes | Palpitations, sweating, dizziness, low serum, glucose | |||||||
Differentiating viral meningitis from other causes of meningitis
Bacterial meningitis may be differntiated from other causes of meningitis by cerebrospinal fluid examination:[21][22][23][24][25]
| Cerebrospinal fluid level | Normal level | Bacterial meningitis[24] | Viral meningitis[24] | Fungal meningitis | Tuberculous meningitis[26] | Malignant meningitis[21] |
|---|---|---|---|---|---|---|
| Cells/ul | < 5 | >300 | 10-1000 | 10-500 | 50-500 | >4 |
| Cells | Lymphos:Monos 7:3 | Gran. > Lymph | Lymph. > Gran. | Lympho.>Gran | Lymphocytes | Lymphocytes |
| Total protein (mg/dl) | 45-60 | Typically 100-500 | Normal or slightly high | High | Typically 100-200 | >50 |
| Glucose ratio (CSF/plasma)[22] | > 0.5 | < 0.3 | > 0.6 | <0.3 | < 0.5 | <0.5 |
| Lactate (mmols/l)[23] | < 2.1 | > 2.1 | < 2.1 | >3.2 | > 2.1 | >2.1 |
| Others | ICP:6-12 (cm H2O) | CSF gram stain, CSF culture, CSF bacterial antigen | PCR of HSV-DNA, VZV | CSF gram stain, CSF india ink | PCR of TBC-DNA | CSF tumour markers such as alpha fetoproteins, CEA |
References
- ↑ Stern TA, Celano CM, Gross AF, Huffman JC, Freudenreich O, Kontos N; et al. (2010). “The assessment and management of agitation and delirium in the general hospital”. Prim Care Companion J Clin Psychiatry. 12 (1): PCC.09r00938. doi:10.4088/PCC.09r00938yel. PMC 2882819. PMID 20582303.
- ↑ 2.0 2.1 Soffer D (1976) Brain tumors simulating purulent meningitis. Eur Neurol 14 (3):192-7. PMID: 1278192
- ↑ 3.0 3.1 Terheggen HG (1985) [CNS tumors with the clinical picture of meningitis.] Monatsschr Kinderheilkd 133 (1):13-9. PMID: 3883130
- ↑ 4.0 4.1 Weston CL, Glantz MJ, Connor JR (2011). “Detection of cancer cells in the cerebrospinal fluid: current methods and future directions”. Fluids Barriers CNS. 8 (1): 14. doi:10.1186/2045-8118-8-14. PMC 3059292. PMID 21371327.
- ↑ 5.0 5.1 Lee MC, Heaney LM, Jacobson RL, Klassen AC (1975). “Cerebrospinal fluid in cerebral hemorrhage and infarction”. Stroke. 6 (6): 638–41. PMID 1198628.
- ↑ Han JH, Wilber ST (2013). “Altered mental status in older patients in the emergency department”. Clin Geriatr Med. 29 (1): 101–36. doi:10.1016/j.cger.2012.09.005. PMC 3614410. PMID 23177603.
- ↑ 7.0 7.1 Birenbaum D, Bancroft LW, Felsberg GJ (2011). “Imaging in acute stroke”. West J Emerg Med. 12 (1): 67–76. PMC 3088377. PMID 21694755.
- ↑ 8.0 8.1 DeLaPaz RL, Wippold FJ, Cornelius RS, Amin-Hanjani S, Angtuaco EJ, Broderick DF; et al. (2011). “ACR Appropriateness Criteria® on cerebrovascular disease”. J Am Coll Radiol. 8 (8): 532–8. doi:10.1016/j.jacr.2011.05.010. PMID 21807345.
- ↑ Stein MT, Trauner D (1982). “The child with a stiff neck”. Clin Pediatr (Phila). 21 (9): 559–63. PMID 7105615.
- ↑ De Cauwer HG, Eykens L, Hellinckx J, Mortelmans LJ (2007). “Differential diagnosis between viral and bacterial meningitis in children”. Eur J Emerg Med. 14 (6): 343–7. doi:10.1097/MEJ.0b013e328270366b. PMID 17968200.
- ↑ Spanos A, Harrell FE, Durack DT (1989). “Differential diagnosis of acute meningitis. An analysis of the predictive value of initial observations”. JAMA. 262 (19): 2700–7. PMID 2810603.
- ↑ Lindquist L, Linné T, Hansson LO, Kalin M, Axelsson G (1988). “Value of cerebrospinal fluid analysis in the differential diagnosis of meningitis: a study in 710 patients with suspected central nervous system infection”. Eur J Clin Microbiol Infect Dis. 7 (3): 374–80. PMID 3137038.
- ↑ Naganuma M, Fujioka S, Inatomi Y, Yonehara T, Hashimoto Y, Hirano T; et al. (2008). “Clinical characteristics of subarachnoid hemorrhage with or without headache”. J Stroke Cerebrovasc Dis. 17 (6): 334–9. doi:10.1016/j.jstrokecerebrovasdis.2008.04.009. PMID 18984423.
- ↑ Rajnik M, Ottolini MG (2000). “Serious infections of the central nervous system: encephalitis, meningitis, and brain abscess”. Adolesc Med. 11 (2): 401–25. PMID 10916131.
- ↑ Tyler KL (2004). “Herpes simplex virus infections of the central nervous system: encephalitis and meningitis, including Mollaret’s”. Herpes. 11 Suppl 2: 57A–64A. PMID 15319091.
- ↑ Kennedy PG (2004). “Viral encephalitis: causes, differential diagnosis, and management”. J Neurol Neurosurg Psychiatry. 75 Suppl 1: i10–5. PMC 1765650. PMID 14978145.
- ↑ Yeh ST, Lee WJ, Lin HJ, Chen CY, Te AL, Lin HJ (2003) Nonaneurysmal subarachnoid hemorrhage secondary to tuberculous meningitis: report of two cases. J Emerg Med 25 (3):265-70. PMID: 14585453
- ↑ Liu LL, Zheng WH, Tong ML, Liu GL, Zhang HL, Fu ZG; et al. (2012). “Ischemic stroke as a primary symptom of neurosyphilis among HIV-negative emergency patients”. J Neurol Sci. 317 (1–2): 35–9. doi:10.1016/j.jns.2012.03.003. PMID 22482824.
- ↑ Berger JR, Dean D (2014). “Neurosyphilis”. Handb Clin Neurol. 121: 1461–72. doi:10.1016/B978-0-7020-4088-7.00098-5. PMID 24365430.
- ↑ Ho EL, Marra CM (2012). “Treponemal tests for neurosyphilis–less accurate than what we thought?”. Sex Transm Dis. 39 (4): 298–9. doi:10.1097/OLQ.0b013e31824ee574. PMC 3746559. PMID 22421697.
- ↑ 21.0 21.1 Le Rhun E, Taillibert S, Chamberlain MC (2013). “Carcinomatous meningitis: Leptomeningeal metastases in solid tumors”. Surg Neurol Int. 4 (Suppl 4): S265–88. doi:10.4103/2152-7806.111304. PMC 3656567. PMID 23717798.
- ↑ 22.0 22.1 Chow E, Troy SB (2014). “The differential diagnosis of hypoglycorrhachia in adult patients”. Am J Med Sci. 348 (3): 186–90. doi:10.1097/MAJ.0000000000000217. PMC 4065645. PMID 24326618.
- ↑ 23.0 23.1 Leen WG, Willemsen MA, Wevers RA, Verbeek MM (2012). “Cerebrospinal fluid glucose and lactate: age-specific reference values and implications for clinical practice”. PLoS One. 7 (8): e42745. doi:10.1371/journal.pone.0042745. PMC 3412827. PMID 22880096.
- ↑ 24.0 24.1 24.2 Negrini B, Kelleher KJ, Wald ER (2000). “Cerebrospinal fluid findings in aseptic versus bacterial meningitis”. Pediatrics. 105 (2): 316–9. PMID 10654948.
- ↑ Brouwer MC, Tunkel AR, van de Beek D (2010). “Epidemiology, diagnosis, and antimicrobial treatment of acute bacterial meningitis”. Clin Microbiol Rev. 23 (3): 467–92. doi:10.1128/CMR.00070-09. PMC 2901656. PMID 20610819.
- ↑ Caudie C, Tholance Y, Quadrio I, Peysson S (2010). “[Contribution of CSF analysis to diagnosis and follow-up of tuberculous meningitis]”. Ann Biol Clin (Paris). 68 (1): 107–11. doi:10.1684/abc.2010.0407. PMID 20146981.
Epidemiology and Demographics
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]
Overview
Viral meningitis affect around 26,000 to 42,000 individual annualy with incidence 11 per 100,000 population. There is no gender or racial predilection.
Epidemiology
- Viral meningitis is associated with an estimated 26.000-42.000 hospitalizations annually in the United States.[1]
- The incidence of the viral meningitis is 11 per 100.000 population per year.
- Enteroviruses are responsible for 85-95% of the viral meningitis cases. They are the cause in the summer and fall seasons.
Demographics
Age
Viral meningitis can occur in any age but it is more common in the infants and children.
Gender
Men and women are affected equally by viral meningitis.
Race
There is no racial predilection for viral meningitis.
Reference
- ↑ Centers for Disease Control and Prevention (CDC) (2003). “Outbreaks of aseptic meningitis associated with echoviruses 9 and 30 and preliminary surveillance reports on enterovirus activity–United States, 2003”. MMWR Morb Mortal Wkly Rep. 52 (32): 761–4. PMID 12917581.
Risk Factors
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]
Overview
Viral meningitis risk factors rely particularly on the exposure to the infection itself and the route of transmission like respiratory droplet and feco-oral transmission. However, there are people at risk to be infected by the disease as children less than 5 years and immunocompromised patients.[1]
Common risk factors
Viral meningitis most common risk factors include the following:
- Children less than 5 years
- Immunocompromised patients
- Direct contact with meningitis patients
- Touching surfaces and objects that were touched by infected patients
Less common risk factors
- Taking chemotherapy medications
- Organ transplant
- Bone marrow transplant
References
- ↑ CDC https://www.cdc.gov/meningitis/viral.html Accessed on April 10, 2017
Screening
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]
Overview
There is no screening for viral meningitis.
Screening
There is no screening for viral meningitis.
References
Natural History, Complications and Prognosis
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]
Overview
Viral meningitis is a self resolved disease if left untreated. It takes around 10 days to be resolved. Seizures and loss of consiousness are the most important complications that may appear in the infants younger than 3 months. It has an excellent prognosis.
Natural history
If left untreated, viral meningitis usually will be self resolved within 10 days. Unlike the bacterial meningitis that may lead to critical medical conditions.
Complications
Although viral meningitis is a self resolved disease in most cases, some complications may take place in the infants younger than 3 months. These complications include the following:[1]
- Seizures
- Loss of consiousness
Prognosis
Viral meningitis prognosis is excellent as the disease usually resolve within 10 days.
References
- ↑ Rorabaugh ML, Berlin LE, Heldrich F, Roberts K, Rosenberg LA, Doran T; et al. (1993). “Aseptic meningitis in infants younger than 2 years of age: acute illness and neurologic complications”. Pediatrics. 92 (2): 206–11. PMID 8337018.
Diagnosis
Diagnosis
History and Symptoms | Physical Examination |Laboratory Findings | CT | MRI | Lumbar Puncture | Other Imaging Findings | Other Diagnostic Studies
Treatment
Treatment
Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
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