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Ankle fractures are common injuries that could result from a  trivial twisting injury in old frail patients up to high energy trauma in a young population. Treatment of these fractures aims to restore joint stability and alignment to reduce the risk of post-traumatic ankle arthritis.[1][2] Anatomy of the Ankle Joint  The ankle joint is a hinge synovial joint that moves in one plane to produce dorsiflexion and plantar flexion.[3] It is formed by the articulation between three bones; distal tibia, distal fibula, and talus bone. The distal tibia and fibula articular portions together form the ankle mortice, which contains the body of talus bone.[3] The ankle joint entires three malleoli; the lateral malleolus (distal end of the fibula), medial malleolus (medial lower end of the tibia), and the posterior malleolus. Ankle joint stability is provided by the ankle mortise articulation with the talus body, the ankle syndesmosis, the ligaments and muscles around the ankle joint. The ankle syndesmosis is a fibrous joint connecting the distal tibia and fibula. The syndesmosis is formed by three main parts; the interosseous tibiofibular ligament, the anterior inferior tibiofibular ligament, and the posterior inferior tibiofibular ligament.[4] The deltoid ligament originates from the medial malleolus and attaches to the talus, navicular, and calcaneus bones and stabilizes the ankle joint against over eversion.[5] The lateral ligaments complex consists of three ligaments originating from the lateral malleolus and attaches to the talus (anterior and posterior talofibular ligaments) and the calcaneus(calcaneofibular ligament). The lateral ligament complex resists the ankle from over the inversion.[5] The ankle joint is innervated by articular branches from the tibial nerve, superficial and deep peroneal nerves. Branches from the peroneal, anterior, and posterior tibial arteries provide the arterial supply to the ankle joint.[6], (Copyright © 2021, StatPearls Publishing LLC.)

Tuberculous meningitis (TBM) is a manifestation of extrapulmonary tuberculosis caused by the seeding of the meninges with the bacilli of Mycobacterium tuberculosis (MTB). MTB is first introduced into the host by droplet inhalation infecting the alveolar macrophage. The primary infection localizes in the lung with dissemination to the lymph nodes.  At this point in the infectious process, there is a high degree of bacteremia that can seed the entire body. In tuberculous meningitis, the meninges are seeded by MTB and form sub-ependymal collections called Rich foci. These foci can rupture into the subarachnoid space and cause an intense inflammatory response that causes meningitis symptoms.  The exudates caused by this response can encase cranial nerves and cause nerve palsies. They can entrap blood vessels causing vasculitis and block cerebral spinal fluid (CSF) flow leading to hydrocephalus. These immune responses can lead to the development of complications associated with tuberculous meningitis and chronic sequela seen in patients who recover from TBM.[1][2], (Copyright © 2021, StatPearls Publishing LLC.)