Understanding the olfactory role in post-COVID cognitive and neuropsychiatric manifestations.

Introduction: Olfactory dysfunction (OD) is frequent after SARS-CoV-2 infection. The aim of this study was to examine if long-term OD is common in post-COVID condition, and the relationship between olfaction, cognition, neuropsychiatric symptoms, and disease duration in these patients. Methods: This study included 121 participants with post-COVID condition and 51 healthy controls (HC). A comprehensive neuropsychological and neuropsychiatric assessment was conducted, encompassing various domains, including general cognition, processing speed, verbal fluency, attention, verbal memory, visual memory, visuoconstructive ability, visuospatial ability, abstraction, executive functions, anxious-depressive symptoms, general health perception, fatigue level, sleep quality, and olfaction. Statistical analyses were carried out to understand the relationship of OD with cognition, and its role as moderator variable. Results: In total, 25% of the post-covid patients had a reduced smell capacity, while only 9.3% of HC presented OD. Post-COVID patients had statistically significantly worse cognitive performance and clinical status than HC. Verbal fluency (AUC = 0.85, p < 0.001), and attention (AUC = 0.82, p < 0.001) were the variables that best discriminate between groups. OD seemed to be a moderator between fatigue and cognition, and between disease duration and attention (ß = -0.04; p = 0.014). Discussion: The study highlights marked cognitive and neuropsychiatric sequelae in individuals post-COVID relative to HC. Olfactory impairment exhibits correlations with both cognitive performance and general health. Olfaction emerges as a potential prognostic marker owing to its moderating influence on disease severity indicators.

Dysautonomia and small fiber neuropathy in post-COVID condition and Chronic Fatigue Syndrome.

BACKGROUND: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and post-COVID condition can present similarities such as fatigue, brain fog, autonomic and neuropathic symptoms. METHODS: The study included 87 patients with post-COVID condition, 50 patients with ME/CFS, and 50 healthy controls (HC). The hemodynamic autonomic function was evaluated using the deep breathing technique, Valsalva maneuver, and Tilt test. The presence of autonomic and sensory small fiber neuropathy (SFN) was assessed with the Sudoscan and with heat and cold evoked potentials, respectively. Finally, a complete neuropsychological evaluation was performed. The objective of this study was to analyze and compare the autonomic and neuropathic symptoms in post-COVID condition with ME/CFS, and HC, as well as, analyze the relationship of these symptoms with cognition and fatigue. RESULTS: Statistically significant differences were found between groups in heart rate using the Kruskal-Wallis test (H), with ME/CFS group presenting the highest (H = 18.3; p ≤ .001). The Postural Orthostatic Tachycardia Syndrome (POTS), and pathological values in palms on the Sudoscan were found in 31% and 34% of ME/CFS, and 13.8% and 19.5% of post-COVID patients, respectively. Concerning evoked potentials, statistically significant differences were found in response latency to heat stimuli between groups (H = 23.6; p ≤ .01). Latency was highest in ME/CFS, and lowest in HC. Regarding cognition, lower parasympathetic activation was associated with worse cognitive performance. CONCLUSIONS: Both syndromes were characterized by inappropriate tachycardia at rest, with a high percentage of patients with POTS. The prolonged latencies for heat stimuli suggested damage to unmyelinated fibers. The higher proportion of patients with pathological results for upper extremities on the Sudoscan suggested a non-length-dependent SFN.

[Sleep disorders in Parkinson's disease: REM sleep behaviour disorder and restless legs syndrome]. / Trastornos del sueño en la enfermedad de Parkinson: trastorno de conducta del sueño REM y síndrome de piernas inquietas.

INTRODUCTION: It is well known that patients with Parkinson's disease (PD) and other neurodegenerative diseases very commonly present sleep disorders, and that they possibly share common pathophysiological mechanisms with motor signs. DEVELOPMENT: In the case of REM sleep behaviour disorder, a number of studies have shown that it may appear more than ten years before the motor signs. Although there is no evidence to prove that patients with restless legs syndrome have an increased risk of suffering from PD, the high prevalence of this symptom in PD and the good response to dopamine agonists suggest the existence of a relation between the two conditions. CONCLUSIONS: The impact that these conditions have on patients' quality of life makes it very important to know how to diagnose and treat them.

[Tics and Gilles de la Tourette syndrome]. / Tics y síndrome de Gilles de la Tourette.

INTRODUCTION: Tourette syndrome is a neurologic disorder characterized by involuntary vocal and motor tics. It affects around 1 to 2% of school-age children and is the most common movement disorder in paediatric age. Tics are involuntary or semivoluntary, sudden, brief, intermittent, repetitive movements (motor tics) or sounds (phonic tics). It is often associated with psychiatric comorbidities, mainly attention-deficit/hyperactivity disorder and obsessive-compulsive disorder. Given its diverse presentation, Tourette's syndrome can almost mimic many hyperkinetic disorders, making the diagnosis challenging at times. DEVELOPMENT: The etiology of this syndrome is thought to be related to basal ganglia dysfunction and many clues have been pursued, both genetic and environmental factors, but no compelling major contribution to the pathogenesis of the disease has yet emerged. Treatment can be behavioural, pharmacologic, or surgical, and is dictated by the most incapacitating symptoms. Alpha-2-adrenergic agonists are the first line of pharmacologic therapy, but dopamine-receptor-blocking drugs are required for multiple, complex tics. Dopamine-receptor-blocking drugs are associated with potential side effects. CONCLUSION: Appropriate diagnosis and treatment can substantially improve quality of life and psychosocial functioning in affected patients.

Tics y síndrome de Gilles de la Tourette / Tics and gilles de la tourette syndrome

Resumen. Introducción. El síndrome de Tourette es un trastorno neurológico caracterizado por múltiples tics motores y vocales. Afecta al 1-2% de los niños en edad escolar y es el trastorno de movimiento más frecuente en edad pediátrica. Los tics son movimientos intermitentes, repetitivos, rápidos y estereotipados, precedidos de una sensación premonitoria que impulsa al realizar el movimiento, se suprimen a voluntad y pueden persistir durante todas las fases del sueño. Frecuentemente se asocian a trastornos neuropsiquiátricos como los trastornos por déficit de atención/hiperactividad y los trastornos obsesivo-compulsivos. Pueden simular casi cualquier trastorno del movimiento. Desarrollo. Se piensa que el origen de la enfermedad está en una disfunción de los ganglios basales, pero a día de hoy no se conocen las causas genéticas o ambientales que la producen. El tratamiento se basa en terapias educacionales, farmacológicas e incluso quirúrgicas en función del síntoma más incapacitante. Los agonistas alfa2-adrenérgicos y los neurolépticos son los fármacos de primera elección. Los neurolépticos deben administrarse con precaución y en dosis bajas debido a sus potenciales efectos adversos. Conclusión. Es importante un tratamiento adecuado de cara a mejorar la calidad de vida y la función psicosocial de los pacientes afectados por esta enfermedad (AU)

Summary. Introduction. Tourette syndrome is a neurologic disorder characterized by involuntary vocal and motor tics. It affects around 1 to 2% of school-age children and is the most common movement disorder in paediatric age. Tics are involuntary or semivoluntary, sudden, brief, intermittent, repetitive movements (motor tics) or sounds (phonic tics). It is often associated with psychiatric comorbidities, mainly attention-deficit/hyperactivity disorder and obsessive-compulsive disorder. Given its diverse presentation, Tourette’s syndrome can almost mimic many hyperkinetic disorders, making the diagnosis challenging at times. Development. The etiology of this syndrome is thought to be related to basal ganglia dysfunction and many clues have been pursued, both genetic and environmental factors, but no compelling major contribution to the pathogenesis of the disease has yet emerged. Treatment can be behavioural, pharmacologic, or surgical, and is dictated by the most incapacitating symptoms. Alpha-2-adrenergic agonists are the first line of pharmacologic therapy, but dopamine-receptorblocking drugs are required for multiple, complex tics. Dopamine-receptor-blocking drugs are associated with potential side effects. Conclusion. Appropriate diagnosis and treatment can substantially improve quality of life and psychosocial functioning in affected patients (AU)