Tuberculous meningitis is a Meninges infection. Meninges are the Tissues Surrounding the Brain and Spinal Cord. It is due to the presence of granulomatous inflammation that leads to the Cerebral Leptomeninges inflammation [1,2]. Mycobacterium Tuberculosis / Koch Bacilli [4] causes tuberculous meningitis. This bacterium is known to cause infectious disease Tuberculosis [1] that usually affects the lungs [3,4], and is a communicable infectious disease [4,10]. It is transmitted through the respiratory tract and primarily affects the lungs but can spread to the brain, bones, eyes and skin via the bloodstream and lymphatic system [14].

Tuberculous meningitis develops in two stages. Mycobacterium Tuberculosis enters the human body through inhalation of a droplet. Localized infection grows rapidly in the lungs and spreads to regional lymph nodes [7], reaching the bloodstream and spreading to other parts of the body. Microtubercles are formed when the bacteria travel to the Meninges (layers that protect the brain) [11] and brain tissue. These Microtubercles can burst and cause Meningitis Tuberculosa. This can be acute or chronic, resulting in increased skull pressure resulting in serious damage to the nerve and brain tissue [8]. The structural portion of Mycobacterium Tuberculosis bacilli is classified as Tuberculosteraic acid [6] (IUPAC: 10 – Methyloctadecanoic acid) [5].


At the initial stage, the Mycobacterium Tuberculosis bacilli enter the human body by droplet inhalation, the initial point of infection being the alveolar macrophage. Localized infection escalates throughout the lung and spreads to primary complex producing area lymph nodes. There is a presence of brief but important bacteremia during this stage which can seed tubercle bacilli into other organs in the human body. For those persons who acquire Tuberculous Meningitis, after the original pathological studies of Rich and McCormick [14], small subpial or subependymal foci called Rich Foci are developed by the bacilli seed to meninges or brain parenchyma [6,12].

The size of the rich concentration is increased during the second stage until it splits into the subarachnoid space [6,12]. This indicates the onset of meningitis which results in serious and irreversible neurological pathology if left untreated [12]. Inflammation is caused by the development of a thick gelatinous exudate which infiltrates the vessels of the cortical or meningeal blood [7]. This exudate develops and spreads along with the growth of focal and diffuse ischemic and brain infarction due to vasculitis, with small proliferating blood vessels. Entrapment of large cerebral arteries, including large artery vasculitis, contributes to infarction.

The exudate envelops the arteries and cranial nerves, resulting in obstruction of cerebrospinal fluid flow at tentorial opening level, leading to hydrocephalus. Tuberculomas can be combined to form granulomas.
Complications of tuberculosis meningitis are hydrocephalus and tuberculoma [14]. Multiple small cerebral and spinal tuberculomas are found when tuberculous meningitis is an indication that military tuberculosis is present [15]. The bacilli may also cross the Blood-Brain Barrier and enter the Cerebro Spinal Fluid (CSF), which helps to control intracranial pressure and functions as a hydraulic shock absorber [10,11].


  • Fever and Chills
  • Altered Sensorium
  • Photophobia (Sensitivity to Light)
  • Severe Headache
  • Stiff Neck (Meningismus)
  • Agitation
  • Unusual Posture
  • Fatigue
  • Lethargy
  • Unconsciousness
  • Loss of appetite
  • Tiredness


  • Excessive ALCOHOL Use
  • Weakened Immune System
  • Diabetes Mellitus
  • Immigrants
  • Children Less than 5 yrs of Age
  • Advancing Age


Proper details, along with medication descriptions, must be given to the patient about the current medical condition. Infection eradication with an increase in signs and symptoms. Because the patient is hypertensive, dietary sodium intake must be limited to 1.5 g / day, with the cessation of alcohol and smoking. Diabetes mellitus and chronic kidney disease are reduced in the amount of sugar and protein intake.


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  13. K. Ilango, P. Valentina. Textbook of Medicinal Chemistry. Vol 2. 2nd ed. Chennai: Keerthi Publishers; 2015. Chapter 4, AntiTubercular agents; p.69
  14. AR Rich, HA McCordick. The pathogenesis of tuberculous meningitis. Bulletin of John Hopkins Hospital 1933;52:5–37
  15. Mei Ling Sharon Tai, Tuberculous Meningitis: Diagnostic and Radiological Features, Pathogenesis and Biomarkers. Neuroscience and Medicine.2013 Jun 18; 4:101-107. doi:10.4236/nm.2013.42016
  16. Garg R. K, Malhotra H. S, Jain A. Neuroimaging in tuberculous meningitis. Neurology India. 2016; 64(2):219-227 doi:10.41030028-3886.177608
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