Meningoencephalitis: Difference between revisions

No edit summary
No edit summary
Line 30: Line 30:
# Mumps virus
# Mumps virus
#[[Human Immunodeficiency Virus (HIV)|HIV]]
#[[Human Immunodeficiency Virus (HIV)|HIV]]
3. [[Parasitic Infections|Protozoal]] Infections
 
* [[Parasitic Infections|Protozoal]] Infections
# Primary amoebic meningoencephalitis, e.g., Naegleria fowleri, Balamuthia mandrillaris, Sappinia diploidea
# Primary amoebic meningoencephalitis, e.g., Naegleria fowleri, Balamuthia mandrillaris, Sappinia diploidea
# Trypanosoma brucei
# Trypanosoma brucei

Revision as of 15:36, 24 April 2023

Original Editor - Kehinde Fatola
Top Contributors - Kehinde Fatola, Reem Ramadan, Kim Jackson and Lucinda hampton

Clinically Relevant Anatomy[edit | edit source]

Meninges are 3 thin layers that cover and protect the brain and spinal cord. They are the dura matter, arachnoid matter and pia matter. These meninges provide a support system for blood vessels, nerves, lymphatics and the cerebrospinal fluid that surrounds your central nervous system[1]. Meningoencephalitis is a neurological condition resembling both meningitis, which is the inflammation of the meninges, and encephalitis, which is the inflammation of the brain tissue[2].

Pathological Process[edit | edit source]

Meningoencephalitis is the result of direct embolization to meningeal vessels, with subsequent parenchymal or cerebrospinal fluid (CSF) invasion of the infecting organism[3]. Meningitis occurs through two routes of inoculation, the first being hematogenous seeding during which bacteria colonize the nasopharynx and enter the bloodstream after the mucosal invasion and make their way to the subarachnoid space, cross the blood-brain barrier causing a direct inflammatory and immune-mediated reaction. The second route of inoculation is direct contiguous spread during which organisms can enter the cerebrospinal fluid (CSF) via neighboring anatomic structures such as otitis media and sinusitis, foreign objects such as medical devices, penetrating trauma, or during operative procedures[4]. Encephalitis occurs from direct viral invasion or as a post-infectious immunologic complication caused by a hypersensitivity reaction to a virus or another foreign protein. These viruses may be epidemic such as poliovirus or sporadic such as herpes simplex and varicella-zoster virus[5].

Meningoencephalitis is caused by various bacterial, viral and protozoan infection.

  1. Listeria monocytogenes
  2. Neisseria meningitidis
  3. Rickettsia prowazekii
  4. Mycoplasma pneumoniae
  5. Tuberculosis
  6. Borrelia (Lyme disease)
  7. Leptospirosis
  1. Tick-borne meningoencephalitis
  2. West Nile virus
  3. Measles
  4. Epstein-Barr Virus
  5. Varicella-zoster virus
  6. Enterovirus
  7. Herpes simplex virus type 1
  8. Herpes simplex virus type 2
  9. Mumps virus
  10. HIV
  1. Primary amoebic meningoencephalitis, e.g., Naegleria fowleri, Balamuthia mandrillaris, Sappinia diploidea
  2. Trypanosoma brucei
  3. Toxoplasma gondii (sporozoa)

Prognosis[edit | edit source]

As the disease is a combination of two very serious neurological conditions, it is linked with severe morbidity and high mortality rate.

Clinical Presentation[edit | edit source]

Patients present with symptoms of both meningitis and encephalitis.

Diagnosis[edit | edit source]

Meningoencephalitis can be dignosed through any of the following like meningitis and encephalitis;

  • Magnetic Resonance Imaging (MRI)
  • Electroencephalography (EEG)
  • Lumbar puncture (spinal tap)
  • Urine analysis
  • Blood test

Management / Intervention[edit | edit source]

Intervention is generally symptomatic and may include various management strategies of meningitis and encephaliti depending on which symptoms are expressed as related to both medical and Physiotherapy managements.

References[edit | edit source]

  1. Greenberg RW, Lane EL, Cinnamon J, Farmer P, Hyman RA. The cranial meninges: anatomic considerations. InSeminars in Ultrasound, CT and MRI 1994 Dec 1 (Vol. 15, No. 6, pp. 454-465). WB Saunders.
  2. Sapra H, Singhal V. Managing meningoencephalitis in indian icu. Indian Journal of Critical Care Medicine: Peer-reviewed, Official Publication of Indian Society of Critical Care Medicine. 2019 Jun;23(Suppl 2):S124.
  3. Aminoff M. Josephson SA. Aminoff's Neurology and General Medicine.6th Edition. Elsevier Science & Technology. 2021.
  4. Feigin RD, MCCRACKEN JR GH, Klein JO. Diagnosis and management of meningitis. The Pediatric infectious disease journal. 1992 Sep 1;11(9):785.
  5. Roos KL. Encephalitis. Neurologic clinics. 1999 Nov 1;17(4):813-33.
  6. Newton PJ, Newsholme W, Brink NS, Manji H, Williams IG, Miller RF. Acute meningoencephalitis and meningitis due to primary HIV infection. British Medical Journal (Clinical research ed.). 2002;325 (7374): 1225–7.
  7. Del Saz SV, Sued O Falcó V, Agüero F Crespo M, Pumarola T, Curran A, Gatell JM.  Acute meningoencephalitis due to human immunodeficiency virus type 1 infection in 13 patients: clinical description and follow-up. Journal of neurovirology. 2008;14 (6): 474–9.