Pathophysiology of Tuberculous Meningitis

       Tuberculous meningitis usually appear as the spread of primary tuberculosis. Usually there is a primary focus of infection in the lungs, but can also be found in the abdomen (22.8 %), neck lymph nodes (2.1 %), with no evidence of primary focus (1.2 %). From the primary focus, the Mycobacteria enter the blood circulation via the thoracic duct and regional lymph nodes, and can cause severe infections such as miliary tuberculosis or just cause some focus metastases are usually quiet.

         Opinion now accepted was stated by Rich in 1951. Occurrence of tuberculous meningitis preceded by her tubercle formation in the brain, the lining of the brain or spinal cord, as a result of hematogenous spread of Mycobacteria during the incubation period of primary infection or during chronic tuberculosis trip though rarely. When hematogenous spread occurs in large numbers, it will immediately cause diseases such as tuberculosis primary tuberculosis meningitis and miliary tuberculosis. Tuberculous meningitis can also be a focus of reactivation of tuberculosis (TB post- primary). One of the originators of the reactivation process is head trauma. Then, Mycobacteria directly into the subarachnoid space or ventricles. Tuberculosis Mycobacteria protein spills into subarachnoid space will stimulate severe hypersensitivity reactions and will further cause inflammatory reactions are most common in the basal brain. Furthermore, a thorough meningitis will develop.

 

Pathologically, there are three circumstances in which it occurs in tuberculous meningitis :
 

1 . Arachnoiditis proliferative
This process mainly occurs in the basal brain , such as the formation of fibrotic mass involving the cranial nerves and then penetrate the blood vessels . Leptomening acute inflammatory reaction in the presence of exudate is characterized by gelatin, yellow-green at the base of the brain. Microscopically, exudate composed of lymphocytes and plasma cells with necrosis caseous. In further stages, exudate will experience the organization and may be hardened and calcified. The cranial nerves are affected will experience paralysis. The most commonly affected nerve is cranial nerve VI, then III and IV, so there will be symptoms of diplopia and strabismus. When the cranial nerve II, the optic chiasm into ischemic symptoms blurred vision and even blindness can occur when the cranial nerves II atrophy of the optic disc. When the cranial nerve VIII will lead to permanent hearing loss.

2. Vasculitis with vascular thrombosis and infarction corticomeningeal across the basement membrane or in the brain parenchyma. This leads to inflammation and subsequent obstruction of cerebral infarction . These abnormalities are left neurological sequelae if the patient survived. When infarction occurs in the area around the media cerebral artery or internal carotid artery, it will arise if infarction is bilateral hemiparese and quadriparese will happen. On histological examination of the affected artery, was found bleeding, proliferation, and degeneration. In the tunica adventitia found infiltration of cells with or without the formation of tubercles and caseous necrosis. In the tunica media is not visible abnormalities, only mild cell infiltration and fibrinoid changes sometimes. Abnormalities in the form of infiltration of subendothelial intima , tunica intima proliferation, degeneration, and caseous. Are commonly affected are the media and the anterior cerebral artery and its branches, and the internal carotid artery. Vein lining of the brain can experience varying degrees of phlebitis and thrombosis and occlusion causes partial or total. The mechanism of phlebitis were not clear, delayed-type hypersensitivity is suspected causes infiltration of mononuclear cells and fibrin changes.
 

3. Communicating hydrocephalus due to extension of inflammation into the cisterna basalis which will disrupt the circulation and cerebrospinal fluid resorption.
The adhesions that occur in the central canal of the spinal cord will cause a spinal block and paraplegia .
Preview pathology that occurs in tuberculous meningitis there are 4 types, namely:
1 . Disseminated milliary tubercles, as in miliary tuberculosis ;
2 . Focal caseous plaques, for example tuberculomas which often causes meningitis is diffuse;
3 . Acute inflammatory meningitis caseous
• Localized, accompanied perkijuan of tubercles, usually in the cortex
• Diffuse, with a gelatinous exudate in the subarachnoid space

4 . Meningitis proliferative
• Localized, in the lining of the brain
• Diffuse with no clear picture
Preview this pathology is not fragmented and may occur simultaneously in each patient. The pathological picture is influenced by several factors, including age, weight and duration of illness, the patient's immune response, duration of response and treatment given, virulence and the number of Mycobacteria is also a factor affecting.