Intracranial pressure (ICP) includes the brain, optic nerve, and spinal cord pressures; it influences blood flow to those structures. Pathological elevation in ICP results in structural damage through various mechanisms, which adversely affects outcomes in traumatic brain injury and stroke. Currently, invasive procedures which tap directly into the cerebrospinal fluid are required to measure this pressure. Recent fluidic engineering modelling analogous to the ocular vascular flow suggests that retinal venous pulse amplitudes are predictably influenced by downstream pressures, suggesting that ICP could be estimated by analysing this pulse signal. We used this modelling theory and our photoplethysmographic (PPG) retinal venous pulse amplitude measurement system to measure amplitudes in 30 subjects undergoing invasive ICP measurements by lumbar puncture (LP) or external ventricular drain (EVD). We estimated ICP from these amplitudes using this modelling and found it to be accurate with a mean absolute error of 3.0 mmHg and a slope of 1.00 (r = 0.91). Ninety-four percent of differences between the PPG and invasive method were between − 5.5 and + 4.0 mmHg, which compares favourably to comparisons between LP and EVD. This type of modelling may be useful for understanding retinal vessel pulsatile fluid dynamics and may provide a method for non-invasive ICP measurement.

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had a waddling gait. Clinical picture was consistent with a clinical diagnosis of LEMS rather than myositis, which was confirmed by elevated anti-VGCC antibodies and response to Acetylcholinesterase inhibitors. Results Anti-VGCC antibodies elevated at 119pM(<30).Transiently elevated CK, negative myositis autoantibodies, negative anti-MuSK antibodies, negative AChR antibodies.Although repetitive nerve stimulation did not show increment in the right ulnar CMAP after isometric muscle activation, the clinical picture was consistent with LEMS.Marked improvement to treatment with oral prednisone and pyridostigmine. Due to side effects, pyridostigmine was changed to 3,4-Diaminopyridine therapy with excellent response.Steroids were weaned off and the patient is adequately controlled on 3,4-Diaminopyridine. Conclusion Our case report shows that LEMS can arise as a result of an immune-related adverse event (irAE) to pembrolizumab; an Anti-PD-1 Monoclonal Antibody. The immune response persists after cessation of this checkpoint inhibitor medication. It is important to recognise and treat this condition early.

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