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Objectives. To evaluate the spectrum of neurological symptoms in patients with COVID-19 during the first 14 days of hospitalisation and its association with in-hospital mortality. Material and methods.We included 200 patients with RT-PCR-confirmed COVID-19 admitted to University Hospital in Krakow, Poland. In 164 patients, a detailed questionnaire concerning neurological symptoms and signs was performed prospectively within 14 days of hospitalisation. In the remaining 36 patients, such questionnaires were completed retrospectively based on daily observations in the Department of Neurology.Results. During hospitalisation, 169 patients (84.5%) experienced neurological symptoms; the most common were: fatigue (62.5%), decreased mood (45.5%), myalgia (43.5%), and muscle weakness (42.5%). Patients who died during hospitalisation compared to the remainder were older (79 [70.5-88.5] vs. 63.5 [51-77] years, p = 0.001), and more often had decreased level of consciousness (50.0% vs. 9.3%, p < 0.001), delirium (33.3% vs. 4.4%, p < 0.001), arterial hypotension (50.0% vs. 19.6%, p = 0.005) or stroke during (18.8% vs. 3.3%, p = 0.026) or before hospitalisation (50.0% vs. 7.1, p < 0.001), whereas those who survived more often suffered from headache (42.1% vs. 0%, p = 0.012) or decreased mood (51.7% vs. 0%, p = 0.003). www.journals.viamedica.pl/neurologia_neurochirurgia_polska Marcin Wnuk et al., Neurological symptoms in COVID-19 Conclusions. Most hospitalised patients with COVID-19 experience neurological symptoms. Decreased level of consciousness, delirium, arterial hypotension, and stroke during or before hospitalisation increase the risk of in-hospital mortality.

A significant number of patients with Gaucher disease (GD) suffer from chronic or acute pain that reduces their quality of life. A mutation in lysosomal enzyme β‐glucosidase (GCase) leads to an accumulation of glucocerebroside in the macrophage‐lineage cells, causing the development of clinical symptoms. Novel studies have revealed that ambroxol (trans‐4‐(2‐amino‐3,5‐dibromobenzylamino)‐cyclohexanol), the well‐known mucolytic drug, acts as a chaperone for the mutant, misfolded enzyme. In addition, as has recently been shown, ambroxol is a Nav1.8 channel blocker in Aβ, Aδ and unmyelinated C fibres, and therefore reduces the transmission of sensory stimuli from the primary afferent neurons to the dorsal spinal cord. In this way, it can act analgetically. Thus, in addition to broncholytic properties, ambroxol combines two other important functions: it enhances enzyme replacement therapy (ERT) and pain management in patients with GD. We present a 38‐year‐old female patient with type 3 GD who had reported permanent bone pain in the lumbar‐sacral part of the spine for over a year without any pathology evidenced in the undertaken, recommended diagnostic tests. The pain was partly controlled with standard analgesics, that is, paracetamol and tramadol. Ambroxol was introduced at a dose of 150mg/d without a noticeable effect. However, when the dose was increased up to 450mg/d, the intensity of pain diminished and subsided within the following months. Two of three attempts to reduce the dose of ambroxol resulted in a pain relapse within a week, which subsided after resetting the previous, higher dose. This observation of the effects of ambroxol in a GD patient is worth considering for other GD patients with chronic pain.

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