Meningoencephalitis

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)

Clinical Presentation[edit | edit source]

Patients present with symptoms of both meningitis and encephalitis. Some of these symptoms include but are not limited to[8]:

  1. Sudden fever
  2. Severe headache
  3. Nausea and vomiting
  4. Double vision and sensitivity to bright light
  5. Stiffness in neck
  6. Confusion, agitation or hallucinations
  7. Loss of sensation or being unable to move certain areas of the face or body
  8. Fatigue or weakness
  9. Loss of consciousness

Diagnostic Procedures[edit | edit source]

The past medical history is necessary during assessment. It's important to obtain relevant information from an accompanying person especially if the patient is agitated, confused or disoriented. In addition to that obtaining past travel history is also crucial due to the possibility of finding specific pathogens from specific geographic locations that cause meningoencephalitis. Meningoencephalitis can be diagnosed through any of the following like meningitis and encephalitis;

  • Magnetic Resonance Imaging (MRI): which is considered extremely sensitive in detecting subtle changes in the early stages of an acute condition although usually patients tend to undergo Computed Tomography (CT) scanning first[9].
  • Electroencephalography (EEG): to demonstrate cerebral involvement during the early state of the disease. It is an indicator of cerebral involvement and usually shows a background abnormality prior to evidence of parenchyma involvement on neuroimaging[10].
  • Lumbar puncture (spinal tap)
  • Urine analysis
  • Blood test: are helpful in separating viral from non-viral pathogens causing the condition[11].

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[12]. People with mild meningoencephalitis usually recover within a few weeks of starting treatment, but in severe cases, nearly 50 to 70% of people will develop secondary brain damage, neurological disorders, or coma[13].

Management[edit | edit source]

The main goals of treating meningoencephalitis are to treat the symptoms and the cause of inflammation. The treatment modality differs according to the type of meningoencephalitis. For example, one of the most common forms of meningoencephalitis is herpes meningoencephalitis where the treatment here involves the administration of an intravenous antiviral medication such as acyclovir, for up to 14 days. It's important to note that the use of these antiviral medications become less effective in later stages of this condition[13]. Another example would be meningoencephalitis caused by bacteria where the treatment here would be intravenous (IV) antibiotics and these antibiotics depend on the causative bacteria. Other types of medications are also prescribed including those that prevent seizers such as dilantin or phenytoin[14]and pain killers. Physical therapy also plays an important role in treatment of complications of this condition such as muscle weakness, poor balance and co-ordination.

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.
  8. Han LL, Popovici F, Alexander Jr JP, Laurentia V, Tengelsen LA, Cernescu C, Gary Jr HE, Ion-Nedelcu N, Campbell GL, Tsai TF. Risk factors for West Nile virus infection and meningoencephalitis, Romania, 1996. The Journal of infectious diseases. 1999 Jan 1;179(1):230-3.
  9. Dale RD, De Sousa C, Chong WK, Cox TC, Harding B, Neville BG. Acute disseminated encephalomyelitis, multiphasic disseminated encephalomyelitis and multiple sclerosis in children. Brain. 2000 Dec 1;123(12):2407-22.
  10. Fowler Å, Stödberg T, Eriksson M, Wickström R. Childhood encephalitis in Sweden: etiology, clinical presentation and outcome. European Journal of Paediatric Neurology. 2008 Nov 1;12(6):484-90.
  11. Kennedy PG. Viral encephalitis: causes, differential diagnosis, and management. Journal of Neurology, Neurosurgery & Psychiatry. 2004 Mar 1;75(suppl 1):i10-5.
  12. Rasul CH, Muhammad F, Hossain MJ, Ahmed KU, Rahman M. Acute meningoencephalitis in hospitalised children in southern Bangladesh. The Malaysian journal of medical sciences: MJMS. 2012 Apr 1;19(2):67-73.
  13. 13.0 13.1 Dash SK. Herpes meningoencephalitis: causes, diagnosis, and treatment. Meningoencephalitis: Disease Which Requires Optimal Approach in Emergency Manner. London, UK: IntechOpen. 2017 Aug 30:49-60.
  14. Temkin NR, Dikmen SS, Wilensky AJ, Keihm J, Chabal S, Winn HR. A randomized, double-blind study of phenytoin for the prevention of post-traumatic seizures. New England Journal of Medicine. 1990 Aug 23;323(8):497-502.