The widespread use of botulinum toxin has been accompanied by an increase in complications, including iatrogenic botulism (IB). This study investigated repetitive nerve stimulation (RNS) findings in IB and myasthenia gravis (MG) patients. Clinical and neurophysiological data were retrospectively reviewed in IB patients negative for both acetylcholine receptor and muscle-specific kinase antibodies, and in MG patients who were positive for either. RNS was performed on the ulnar nerve at 2, 3, 5, and 50 Hz, and on the facial and spinal accessory nerves at 2, 3, and 5 Hz. Fifteen IB and 23 MG patients were included. Compound muscle action potential (CMAP) amplitudes of the ulnar and facial nerves were lower in IB (p = 0.014, p = 0.006). A progressive decrement at low-frequency RNS occurred in 60% of IB and 17% of MG patients. At 5 Hz facial RNS, 1st-2nd (p = 0.044) and 1st-4th (p = 0.008) decrements were greater in MG, whereas the 4th-10th decrement was higher in IB (p = 0.031). Ulnar CMAP changes at 50 Hz were greater in IB (p < 0.001); nine patients showed increments > 40%, four > 60%, and one > 100%, while none of the MG patients exceeded 40%. Reduced CMAP amplitude, an incremental response at high frequency, and a progressive decrement at low frequency were more commonly encountered in IB. In MG, a U-shaped pattern at low frequency and a more pronounced decrement between the 1st and 2nd responses were noted.

Botulinum toxin (BT) is infamous for its extreme toxicity. If it enters the bloodstream, it can cause botulism presenting with a typical pattern of motor and autonomic dysfunction. An international expert panel organised by IAB-Interdisciplinary Working Group for Movement Disorders explored iatrogenic botulism after BT's medical use (IB), reached conclusions and formulated recommendations. When injected into its target tissue, BT binds to gangliosides on cholinergic nerve terminals before it is internalised permanently. Small amounts of BT, however, are circulating within the bloodstream. When BT type B is applied, IB-B occurs frequently, typically affecting the autonomic nervous system. When BT type A is applied, IB-A only occurs in special circumstances, even when high doses are used. We identified 236 patients with IB-A in the literature. All IB-A was mild or moderate and fully reversible. In 212 patients, it occurred with unapproved BT use. In 116 of them, unapproved BT preparations were used, in 81, unapproved indications were treated and in 15, underlying neuromuscular impairment including myasthenia gravis, Lambert-Eaton myasthenic syndrome, amyotrophic lateral sclerosis and spinal muscle atrophy were contraindications for BT use. In 24 patients, IB-A occurred in approved BT use. Their evaluation was frequently incomplete, so that causes for IB-A often remain unclear. They may include presence of differential diagnosis, subclinical neuromuscular impairment and interference with additional diseases. When IB is suspected, proper evaluation is necessary to verify it and to identify its causes. Off-label use is common in BT therapy. However, it should be performed with caution, especially in children and when high doses are applied. High BT doses should not be applied to low volumes of target tissues, in order not to exceed the BT binding capacity.

BackgroundBotulinum toxin is widely used for the treatment of spasticity in pediatric patients with cerebral palsy. Although regarded as safe, rare but severe systemic complications, such as iatrogenic botulism, may arise.Case PresentationWe present the case of an 8-year-old boy with cerebral palsy who experienced global muscle weakness, bilateral ptosis, dysphagia, and respiratory distress after botulinum toxin A (Dysport). The clinical presentation was consistent with iatrogenic botulism. The patient was administered botulinum antitoxin, resulting in a gradual enhancement of the condition. Sequential clinical photos depict the progression of the sickness and subsequent recovery, which led to progressive improvement.ConclusionIatrogenic botulism must be contemplated in individuals exhibiting new-onset bulbar or respiratory symptoms after botulinum toxin injection. Timely identification and prompt commencement of antitoxin treatment are essential for positive outcomes.

Botulinum toxin (BoNT) is extensively used across a wide range of therapeutic and cosmetic applications due to its efficacy in inhibiting neuromuscular transmission and its well-established safety profile. While adverse effects are typically localized and transient, systemic complications - particularly iatrogenic botulism - are rare but potentially life-threatening events. Iatrogenic botulism results from unintended systemic spread of the neurotoxin, which can occur even at doses commonly used for cosmetic purposes. We report a rare and severe case of iatrogenic botulism in a previously healthy 47-year-old male who developed progressive neurological symptoms following cosmetic BoNT injections to the glabellar region. Within days of the procedure, the patient experienced worsening bilateral ptosis, ophthalmoplegia, dysarthria, and dysphagia, which progressed to respiratory muscle involvement requiring mechanical ventilation in an intensive care setting. Neurophysiological studies demonstrated findings consistent with a presynaptic neuromuscular transmission defect. The case presented several diagnostic challenges, as the early clinical features mimicked other neuromuscular disorders such as myasthenia gravis or brainstem stroke. Despite this, prompt recognition based on clinical suspicion led to the timely administration of heptavalent botulinum antitoxin, which was followed by gradual neurological improvement. This case underscores the importance of early identification and management of systemic BoNT toxicity, even in the context of routine cosmetic use. It also highlights the critical need for clinician awareness, early referral to specialized care, and a high index of suspicion in patients presenting with acute cranial neuropathies following BoNT administration. This report aims to highlight the potential for severe systemic complications associated with BoNT use and to emphasize the importance of early antitoxin administration.

We report the case of a 35-year-old woman who developed progressive neuromuscular weakness, bulbar symptoms, and dysphagia following administration of unlicensed cosmetic botulinum toxin at home by a non-medical acquaintance. Her husband, who received injections from the same vial, was admitted to intensive care and required intubation. Our patient required close airway monitoring, antitoxin therapy, immunoglobulins, and multidisciplinary support, but did not require ventilatory support. She gradually improved and was discharged with ongoing outpatient neurology and speech therapy follow-up. This case highlights the dangers of unregulated access to botulinum toxin, the importance of early recognition of iatrogenic botulism, and the role of public health reporting in preventing further harm.