Cerebrospinal fluid and serum interleukins 6 and 8 during the acute and recovery phase in COVID-19 neuropathy patients.

This case series describes three patients affected by severe acute respiratory syndrome coronavirus 2, who developed polyradiculoneuritis as a probable neurological complication of coronavirus disease 2019 (COVID-19). A diagnosis of Guillain Barré syndrome was made on the basis of clinical symptoms, cerebrospinal fluid analysis, and electroneurography. In all of them, the therapeutic approach included the administration of intravenous immunoglobulin (0.4 gr/kg for 5 days), which resulted in the improvement of neurological symptoms. Clinical neurophysiology revealed the presence of conduction block, absence of F waves, and in two cases, a significant decrease in amplitude of compound motor action potential cMAP. Due to the potential role of inflammation on symptoms development and prognosis, interleukin-6 (IL-6) and IL-8 levels were measured in serum and cerebrospinal fluid during the acute phase, while only serum was tested after recovery. Both IL-6 and IL-8 were found increased during the acute phase, both in the serum and cerebrospinal fluid, whereas 4 months after admission (at complete recovery), only IL-8 remained elevated in the serum. These results confirm the inflammatory response that might be linked to peripheral nervous system complications and encourage the use of IL-6 and IL-8 as prognostic biomarkers in COVID-19.

Alpha-ketoglutaramate: increased concentrations in the cerebrospinal fluid of patients in hepatic coma.

alpha-Ketoglutaramate, a deaminated metabolite of glutamine not previously identified in biological tissues, was measured in the cerebrospinal fluid of human subjects and found to be increased three- to tenfold in patients with hepatic coma. When perfused into the cerebral lateral ventricles of rats, alpha-ketoglutaramate (10 mM) depressed the animals' nocturnal locomotor activity, and at higher doses induced circling behavior and myoclonus. The concentration of alpha-ketoglutaramate in cerebrospinal fluid appears to be a reliable diagnostic indicator of hepatic coma, and its accumulation may contribute to the pathogenesis of this disease.

Biochemical changes in acute respiratory failure.

A study has been carried out on patients presenting respiratory failure from chronic obstructive lung disease. Acid-base balance, electrolytes and amino acids levels have been studied in plasma and in cerebrospinal fluid (CSF) of patients in hypercapnic coma and results compared with those observed in patients with primary acute hypercapnia. Additional cardiopulmonary measurements were made. The study has shown evidence of significant modification of the distribution ratios of plasma and CSF electrolytes and amino acids, particularly in the patients with coma. The changes seem to be related to variations of the transmembrane potentials and alterations of some metabolic pathways involved in the homeostasis and in neurotransmission. Finally some of the changes of amino acid in plasma and CSF appear significantly correlated to variations in pulmonary function and to modification of acid-base balance observed both in plasma and CSF.

Correlation between acid-base status, concentrations of lactate and of pyruvate in blood and cerebrospinal fluid in patients treated in an intensive care unit.

Results of examinations of 41 patients treated in an intensive care unit are reported. The patients were divided into three groups and examined on the first and twelfth days of treatment. In the first group were 15 patients who had received circulatory resuscitation, the second group was 13 patients with lesions of the central nervous system of traumatic or vascular origin and the third group was 13 patients with acute respiratory insufficiency of toxic or infective origin. The cerebrospinal fluid of patients in the second group showed the lowest pH (mean pH 7.28) and bicarbonate concentration (19.05 mequiv./1); this group also had the lowest PO2 values. Moderate respiratory alkalosis was observed in the arterial blood of patients with lesions of the central nervous system. Concentrations of lactate in the cerebrospinal fluid were increased in all three groups of patients although blood lactate concentrations were normal. The lactate/pyruvate concentration ratio was highest in the resuscitated patients.

[Clinical course and treatment of acute inflammatory demyelinating polyradiculoneuropathy (Landry-Guillain-Barré syndrome)]. / Klinika i lechenie ostroi vospalitel'noi demieliniziruiushchei poliradikuloneiropatii (sindroma Landri-Giiena-Barre).

Motor, sensitive and vegetative disorders were subjected to a clinical analysis in 40 adult patients with Landry-Guillain-Barre syndrome in the acute disease stage and during rehabilitation. Investigation of the cerebrospinal fluid and of the rate of the nervous impulses conduction in the peripheral nerves has demonstrated that in the majority of the patients, the clinical findings did not correlate with the laboratory ones. Early diagnosis and rational therapy with plasmapheresis and glucocorticoids ensured a favourable prognosis.

The reversal of the oxygen difference between arterial blood and cerebrospinal fluid in chronic, exacerbated respiratory insufficiency.

The relationship between PaO2 and PCSFO2 (along with other acid-base parameters) was studied in patients with long-lasting respiratory failure. These patients exhibited a highly significant reversal of the normal relationship, i.e. their PCSF O2 was invariably higher, than PaO2. It is suggested that this reflects a mechanism protecting the brain against hypoxia.

Relapsing-remitting autoimmune agrypnia.

A woman affected by multiple cranial nerve palsy developed several episodes of total insomnia and respiratory crises resulting from central breathing depression associated with dysautonomic symptoms. Oligoclonal IgG bands were present in her cerebrospinal fluid, and immunohistochemistry showed increased binding of serum and cerebrospinal fluid on gamma-aminobutyric acid-ergic, synapse-rich neuronal cells. Immunosuppressive treatment and plasma exchange were followed by clinical improvement, with restoration of sleep architecture and disappearance of respiratory crises, suggesting autoimmune pathogenesis of the syndrome.