The neuroprotective potential of stingless bee honey (SBH) is still to be documented from numerous studies including that of its effect on cerebrovascular event. This review should guide stroke rehabilitation specialties to a high understanding of the overall circuit changes post-stroke, the clinical relevance of this change in stroke to cognitive impairment and dementia, and SBH as a supplementation in modern stroke rehabilitation in progresses. However, the potential of SBH as a supplementation therapy and highlights treatment to induced plasticity for post-stroke vascular cognitive impairment (PSVCI) remains largely unexplored. This Chapter attempts to deliberate on recent evidence that highlight the therapeutic properties of honey and SBH, the features of PSVCI, and proposing the plausible mechanism of action for SBH as a supplementation during stroke rehabilitation that could halt the progression of PSVCI. It is hoped that such an approach could complement the existing evidence-based stroke care, and which will help in the development of future direction of brain plasticity to delay the progression of cognitive impairment post-stroke.

Introduction: Distal renal tubular acidosis (RTA) is easily recognized in patients with hypokalemia and normal anion gap acidosis. Other concurrent electrolyte abnormalities could change the diagnosis. We describe a newly diagnosed distal RTA complicated with severe hypernatremia and hypophosphatemia while admitted to the intensive care unit. Case report: A 12-year-old girl presented with worsening paralysis. Initial investigations revealed low serum potassium of 1.8mmol/L, pH 7.2mmol/L, bicarbonate 12mmol/L and high urine pH (8.0) suggesting distal RTA. She required mechanical ventilation due to severe metabolic acidosis and hypokalemia. Resuscitation strategies initially focussed on intravenous hydration with 0.9% normal saline and potassium repletion. Delayed correction of acidosis with sodium bicarbonate led to severe hypernatremia (180mmol/L) and slow recovery of serum potassium level. Hypernatremia was also contributed by concurrent nephrogenic diabetes insipidus. Interestingly, her serum phosphate was persistently low (0.4mmol/L) leading to more workup to investigate proximal tubulopathy. It persisted till resolution of hypernatremia and acidosis. Meanwhile she developed sepsis with multiple thromboses attributed to disseminated tuberculosis. Screening for connective tissue diseases were negative. She recovered well and was discharged with anti-tuberculosis drugs, anticoagulation and potassium supplements. Conclusion: In conclusion, correction of acidosis in distal RTA should be prioritised to avoid prolonged hypokalemia and significant increase in serum sodium. Hypophosphatemia in a critically ill patient should be interpreted with caution, correlating with serum sodium and arterial blood gas to avoid incorrect diagnoses.