Severe foodborne botulism: patterns of neurophysiological changes during the acute phase of the disease

Foodborne botulism is a rare, acute neuromuscular disorder of infectious-toxic origin, caused by the neurotoxin produced by Clostridium botulinum. In severe cases of foodborne botulism, characterized by the acute onset of flaccid tetraparesis, severe oculomotor and bulbar disorders, there are reasonable difficulties in differential diagnosis with phenotypically similar diseases– Guillain–Barre syndrome and autoimmune myasthenia gravis. In this regard, a detailed description of the neurophysiological changes associated with botulism is essential, as this will facilitate the differential diagnostic process and enable a correct diagnosis to be established in a timely manner. Objective: to demonstrate the pattern of neurophysiological changes in patients with severe foodborne botulism during the acute phase. Material and methods. The study included 27 patients. The inclusion criteria were a confirmed diagnosis of ‘foodborne botulism’, the acute phase (disease duration of less than 14 days) and a severe form of the disease (requiring mechanical ventilation). The study methods included an analysis of discharge summaries and a neurophysiological examination to assess the conduction function of the long limb nerves, with an examination of the deltoid muscle using a needle electrode, a decrement test, and analysis of the jitter of the orbicularis oculi muscle. Results. In patients with severe foodborne botulism during the acute phase, no disturbances in conduction function and/or damage to the axons of motor and sensory fibers of the peripheral nerves of the limbs were detected. Low-amplitude motor responses were recorded from the paretic muscles (facial and bulbar groups); the degree of paresis of the orbicularis oculi muscle correlated with the M-response amplitude from this muscle (p<0.04). The mean parameters of motor unit potentials recorded in the deltoid muscle were within the age-related normal range; in some patients, isolated spontaneous activity of muscle fibres was recorded. A pathological (greater than 10%) decrease in the amplitude of the motor response from the paretic muscles was not recorded in all patients: in 55% of cases (n=15) – from the orbicularis oculi muscle; in 41% of cases (n=11) – from the rectus abdominis muscle; and in only 7% of patients (n=2) – from the trapezius muscle; furthermore, it did not correlate with the severity of muscle weakness. A pathological (greater than 50%) increase in the amplitude of the motor response during tetanization was observed in the abductor pollicis brevis muscle in 6 (22%) patients and in the abductor digiti minimi muscle in 13 (48%) patients. In 100% of patients in the analyzed sample, an increase in the jitter of the orbicularis oculi muscle of varying degrees was noted. Conclusion. The analysis of jitter of the facial muscles proved to be the most informative method for verifying neuromuscular transmission disorders in patients with severe foodborne botulism. The low amplitude of the motor response and the absence of pathological changes in half of the patients during decrement and increment tests of the paretic muscles are due to the severity of the neuromuscular transmission disorder – a severe presynaptic block. It should be borne in mind that all recorded neurophysiological changes in severe foodborne botulism are non-specific and must be considered strictly in combination with clinical and anamnestic data. The data obtained from this study will help to improve the differential diagnosis of acute flaccid tetraparesis syndrome and enable the timely confirmation of foodborne botulism.