Low vitamin B12 status is common in older people; however, its public health significance in terms of neurological manifestations remains unclear. The present systematic review evaluated the association of vitamin B12 status with neurological function and clinically relevant neurological outcomes in adults aged 50+ years. A systematic search of nine bibliographic databases (up to March 2013) identified twelve published articles describing two longitudinal and ten cross-sectional analyses. The included study populations ranged in size (n 28–2287) and mean/median age (range 65–81 years). Studies reported various neurological outcomes: nerve function; clinically measured signs and symptoms of nerve function; self-reported neurological symptoms. Studies were assessed for risk of bias, and results were synthesised qualitatively. Among the general population groups of older people, one longitudinal study reported no association, and four of seven cross-sectional studies reported limited evidence of an association of vitamin B12 status with some, but not all, neurological outcomes. Among groups with clinical and/or biochemical evidence of low vitamin B12 status, one longitudinal study reported an association of vitamin B12 status with some, but not all, neurological outcomes and three cross-sectional analyses reported no association. Overall, there is limited evidence from observational studies to suggest an association of vitamin B12 status with neurological function in older people. The heterogeneity and quality of the evidence base preclude more definitive conclusions, and further high-quality research is needed to better inform understanding of public health significance in terms of neurological function of vitamin B12 status in older people.

Neuromuscular complications encountered in intensive care can be due to peripheral nerves (polyneuropathies), muscles (myopathies), neuromuscular end-plate (transmission deficit) or a combination of these. Neurophysiopathological tests that enable us to diagnose and maybe differentiate between these causes are essentially electroneurographs and electromyographs. These assess, either directly or indirectly, the integrity of the peripheral system, both sensory (centripetal afferent pathways) and motor (lower motor neurones, neuromuscular junction, muscle membrane and contractile substrate). Electrical activity in the muscle is measured using a special device (an electromyograph) comprising preamplifiers, a computer with special programmes and algorithms for analysing, digitalizing, amplifying and filtering the recorded signal and a monitor on which to visualize the on-line trace. The machine also has speakers. These serve to recognize and identify the physiological events being recorded as they make such unusual, individual sounds. An electric stimulator with constant current can be used to stimulate branches of superficial nerves (motor, sensory or mixed) so that electric conduction speed can be studied and the sensory or motor response analysed. The results can be saved on a hard disc or on any magnetic or digital support, viewed off-line or even printed.

Routine motor nerve conduction studies measure latencies, conduction velocities and amplitudes of compound action potentials. These measurements can be very useful in defining the pathology, while they provide little insight into the underlying disease mechanisms. Increasingly, the technique of ‘threshold tracking’ is being used in research and clinical studies on large myelinated axons. Nerve excitability testing is a non-invasive approach in investigating the pathophysiology of peripheral nerve disorders, which determines the electrical properties of the nerve membrane at the site of stimulation. We have found evidence that in patients with critical illness polyneuropathy peripheral nerves are depolarized. The correlations with serum factors suggest that this membrane depolarization is related to endoneurial hyperkalemia and/or hypoxia. While other mechanisms of depolarization may well be involved, the degree to which potential-sensitive nerve excitability indices are related to serum potassium and bicarbonate suggests that other factors, independent of potassium and acid–base balance, are likely to be of relatively minor significance.