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Pathogenesis Primary brain stem injury is the result of the direct effect of the trauma which results in its distortion and displacement. Kalyanaraman and Ramamurthi (1969) reported 42 cases of brain stem injury among 1100 cases of head injury patients admitted to their head injury unit in 18 months.[[1]] As late at 2007, Shukla et al. stated, "Several autopsy studies of head injury are available, but pathology of brain stem and hypothalamus injury are addressed in very few of them. "In many general surgical works today the diagnosis of primary brain stem injury amounts to pronouncement of death sentence" (Kalyanaraman and Ramamurthi 1969) It is interesting that around the same time as the above statement on ominous saying in some centers in Delhi acquired a similar predicament, "Yeh to brain stem ho gaya ab iska kuch nahi ho sakta" (He has become brain stem, now nothing can be done about it). While brain stem hemorrhage is more common in the secondary group of brain stem lesions, these are not uncommon in the primary injury especially in the lateral part of the mid-brain, the superior cerebellar peduncle, and rostral pons. [Extracted from the article]

Background: Mycobacterium tuberculosis (MTB) in latent infection has been demonstrated in pulmonary/extra‐pulmonary locations (lung, spleen, liver, kidney, adipose tissue) in autopsy studies, but its presence in ocular tissues in the latent state is not known. Methods: We conducted molecular and histopathological study of 100 cadaver eyes (50 humans) who died from causes other than tuberculosis (TB) (and were potential candidates for corneal transplantation) to detect MTB in ocular tissues in an endemic setting. After removal of the corneal button, an 8 to 10 mm block of tissue (choroid, retina and part of the vitreous) was excised from the remaining globe for DNA isolation. Gel‐based IS6110 and devR3 polymerase chain reaction (PCR) assays were done, followed by real‐time PCR using beta actin gene as an internal control. Sixteen randomly selected DNA samples were double checked using a commercial kit for MTB and non‐tuberculous mycobacteria (NTM) DNA. The remaining larger part of the globe was subjected to histopathology. Results: The mean age was 65.14 ± 18 years. All 100 samples were negative for both IS6110 and devR, and all 16 samples were negative with NTM MTB commercial kit. All samples were negative with Ziehl‐Neelsen stain for acid fast bacilli and none showed any inflammation or granulomatous pathology. Conclusions: MTB could not be detected in human ocular tissues in latent state in India, a TB‐endemic country. This may suggest the inability of MTB to seed ocular tissues in the latent state, unlike other organs which serve as reservoirs for the bacilli in the absence of manifest disease. [ABSTRACT FROM AUTHOR]