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Tuberculosis remains a global health problem, with an estimated 10.4 million cases and 1.8 million deaths resulting from the disease in 2015. The most lethal and disabling form of tuberculosis is tuberculous meningitis (TBM), for which more than 100,000 new cases are estimated to occur per year. In patients who are co-infected with HIV-1, TBM has a mortality approaching 50%. Study of TBM pathogenesis is hampered by a lack of experimental models that recapitulate all the features of the human disease. Diagnosis of TBM is often delayed by the insensitive and lengthy culture technique required for disease confirmation. Antibiotic regimens for TBM are based on those used to treat pulmonary tuberculosis, which probably results in suboptimal drug levels in the cerebrospinal fluid, owing to poor blood-brain barrier penetrance. The role of adjunctive anti-inflammatory, host-directed therapies - including corticosteroids, aspirin and thalidomide - has not been extensively explored. To address this deficit, two expert meetings were held in 2009 and 2015 to share findings and define research priorities. This Review summarizes historical and current research into TBM and identifies important gaps in our knowledge. We will discuss advances in the understanding of inflammation in TBM and its potential modulation; vascular and hypoxia-mediated tissue injury; the role of intensified antibiotic treatment; and the importance of rapid and accurate diagnostics and supportive care in TBM.

Diabetic neuropathy (DN) refers to symptoms and signs of neuropathy in a patient with diabetes in whom other causes of neuropathy have been excluded. Distal symmetrical neuropathy is the commonest accounting for 75% DN. Asymmetrical neuropathies may involve cranial nerves, thoracic or limb nerves; are of acute onset resulting from ischaemic infarction of vasa nervosa. Asymmetric neuropathies in diabetic patients should be investigated for entrapment neuropathy. Diabetic amyotrophy, initially considered to result from metabolic changes, and later ischaemia, is now attributed to immunological changes. For diagnosis of DN, symptoms, signs, quantitative sensory testing, nerve conduction study, and autonomic testing are used; and two of these five are recommended for clinical diagnosis. Management of DN includes control of hyperglycaemia, other cardiovascular risk factors; alpha lipoic acid and L carnitine. For neuropathic pain, analgesics, non-steroidal anti-inflammatory drugs, antidepressants, and anticonvulsants are recommended. The treatment of autonomic neuropathy is symptomatic.

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There is a paucity of large studies evaluating the subtypes of Guillain-Barré syndrome (GBS) and their outcome from Southeast Asia. We report cliniconeurophysiological subtypes of GBS and their correlation with triggering events and 3-month outcome from northern India. Three hundred and twenty eight consecutive patients with GBS were clinically evaluated, including their triggers, severity, autonomic involvement, cranial nerve palsy, and respiratory paralysis. Nerve conduction study (NCS) was repeated at 3 weeks if the initial study was normal. They were categorized into acute inflammatory demyelinating polyradiculoneuropathy (AIDP), acute motor axonal neuropathy (AMAN), acute motor sensory axonal neuropathy (AMSAN), inexcitable motor nerve, and equivocal. Clinically, 204 (62.2%) patients had pure motor, 106 (32.3%) motor sensory, 16 (4.9%) Miller Fisher syndrome, and 2 (0.6%) pure sensory GBS. Based on NCS, 242 (73.8%) had AIDP, 44 (13.4%) AMAN, 15 (4.6%) AMSAN, 8 (2.4%) inexcitable motor nerves, and 27 (8.2%) equivocal GBS. AIDP patients were older, more common in summer, had lesser peak disability, and better outcome compared to those with AMAN. Eleven (3.4%) patients died and 48 (14.6%) had poor outcome at 3 months. The poor outcome was related to severity, dysautonomia, and inexcitable motor nerves. AIDP is the commonest variant of GBS in our study and has better outcome compared to AMAN.