The immunoprotective role of pregnancy in multiple sclerosis (MS) has been known for decades. Conversely, there has been rich debate on the topic of breastfeeding and disease activity in MS. In clinical practice, women are often offered to restart their disease-modifying drug (DMD) soon after delivery to maintain their relapse risk protection. Limited available information about peri-partum DMD safety can discourage women to choose breastfeeding, despite the World Health Organization's recommendation to breastfeed children for the first 6 months of life exclusively. New evidence is emerging about the protective role of exclusive breastfeeding on relapse rate. Research studies shed light on the hormonal and immunological mechanisms driving the risk of relapses during pregnancy and postpartum. Finally, case reports, real-world data, and clinical trials are increasing our knowledge of the safety of DMDs for the fetus and infant. While some DMDs must be avoided, others may be considered in highly active pregnant or lactating women with MS. This mini-review conveys recent evidence regarding the protective role of exclusive breastfeeding in MS and offers clinicians practical considerations for a patient-tailored approach.

A 60-year-old woman was referred to the Autonomic Centre at the National Hospital for Neurology and Neurosurgery (NHNN) due to longstanding history of orthostatic hypotension (OH).She was born of non-consanguineous parents and there was no family history of similar problems. Her tolerance for exercise has been significantly low since childhood.She has a background of schizophrenia, chronic kidney disease and cardiac arrythmias.She was first seen at the NHNN 30 years earlier and investigated with skin biopsy showing loss of tyrosine hydroxylase and neuropeptide Y.During a recent admission, the neurologic examination showed bilateral Horner’s syndrome, OH and parkinsonism (possibly drug induced). Autonomic tests indicated selective impairment of adrenergic sympathetic function. Plasma adrenaline, noradrenaline, dopamine and dopamine beta hydroxylase (DβH) levels were undetectable.The patient is currently being investigated for mutations in genes encoding DβH and CYB561. DβH mutation is unlikely due to the undetectable dopamine. CYB561 gene mutation has been described to interfere with noradrenaline biosynthesis, resembling DβH deficiency.Both disorders are characterised by orthostatic hypotension, recurrent hypoglycaemia and low noradrena- line levels. Establishing the aetiology might have an impact on management given the response to L-DOPS in patients with mutation of genes involved in noradrenaline biosynthesis.16sk0577cam@gmail.com