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1.
Cureus ; 15(11): e48964, 2023 Nov.
Article in English | MEDLINE | ID: mdl-38106719

ABSTRACT

Botulism is a rare cause of flaccid paralysis resulting from the neurotoxin produced by the bacterium Clostridium botulinum. It is clinically characterized by symmetric proximal-distal paralysis, diplopia, dysarthria, dysphonia, and dysphagia. Definitive diagnosis requires laboratory confirmation through the detection of the toxin in blood, vomit, or stool samples. Treatment with antitoxin should be promptly initiated upon clinical suspicion and in the presence of epidemiological support due to evidence of reduced mortality. Physical and rehabilitation medicine plays a fundamental role in the recovery of deficits and prevention of complications. In this report, the authors describe a 19-year-old patient with botulism with dysphagia, dysphonia, and facial paresis in the rehabilitation ward.

2.
Cureus ; 15(9): e45423, 2023 Sep.
Article in English | MEDLINE | ID: mdl-37854764

ABSTRACT

Guillain-Barré syndrome (GBS) stands as one of the primary causes of acute flaccid paralysis. It includes acute-onset peripheral nerve lesions and typically follows a monophasic course. Its etiopathogenesis is linked to an immune-mediated response to a prior infection, often respiratory or intestinal. The main variants of GBS are acute inflammatory demyelinating polyneuropathy, which accounts for approximately 90% of cases in the USA and Europe, and acute motor axonal neuropathy, responsible for about 10% of cases in the USA and Europe. From the literature review, only one case of GBS preceded by hand, foot, and mouth disease (HFMD) has been described. The authors report a rare clinical case of typical GBS after HFMD. Recognizing this adult-onset disease as a potential preceding infection of GBS is crucial for early diagnosis and treatment. Additionally, the integration into a rehabilitation program adjusted to the deficits plays an important role in motor and functional recovery.

4.
Cureus ; 14(12): e32655, 2022 Dec.
Article in English | MEDLINE | ID: mdl-36654564

ABSTRACT

BACKGROUND: The clinical presentation of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can range from mild or moderate disease (80% of the cases) to severe disease (15%) requiring oxygen support, and critical disease (5%), associated with acute respiratory distress syndrome and admission to the intensive care unit (ICU). In critically ill patients, prone positioning can be used to optimize oxygenation. Although there is a favourable response to this strategy, being a life-saving measure, additional associated complications may appear, including compressive neuropathies. Despite respiratory affection being more common, SARS-CoV-2 infection can also attack other systems and can, under certain conditions, affect the central or peripheral nervous system. It has been described that neurological manifestations can result from the neuroinvasive properties of the SARS-CoV-2 or as an indirect consequence of multiorgan dysfunction. AIMS: We intend to report the patients who presented with neurological complications associated with coronavirus disease 2019 (COVID-19) and/or complications of its treatment, followed in our physical and rehabilitation medicine (PRM) service. MATERIALS AND METHODS: A retrospective analysis of patients admitted to the PRM ward with outpatient consultation in the context of post-COVID-19 status between April 2020 and November 2021 (the period of the highest prevalence of infection) was carried out. Patients with neurological complications after SARS-CoV-2 infection and consequently a decline in previous functionality were identified. RESULTS: Thirteen patients (23.6%) admitted to the PRM ward had peripheral neurological complications, documented by electroneuromyography, including Guillain-Barré syndrome, sensory-motor polyneuropathy, peroneal nerve injury, femoral nerve injury, and lumbar plexus injury. The neurological complications of the patients followed in a post-COVID-19 consultation were also evaluated. Eight patients (20%) reported neurological sequelae. Five patients presented peripheral nerve damage (peroneal, accessory, ulnar, and recurrent laryngeal) of undefined aetiology, diagnosed after the acute phase of hospitalization. Two patients had COVID-19 infection followed by ischemic stroke (vertebrobasilar and middle cerebral artery), requiring hospitalization in the acute phase. One patient had COVID-19 infection followed by longitudinal myelitis, with positive anti-myelin oligodendrocyte glycoprotein (MOG). All patients required follow-up by the rehabilitation team with partial recovery of deficits. CONCLUSIONS:  All patients admitted to the PRM ward with neurological manifestations had critical disease and symptoms compatible with peripheral nervous system involvement. Patients admitted to the PRM consultation had different levels of viral disease severity and had sequelae related to peripheral and central nervous system disorders. Identifying the aetiology of these injuries is essential for us to act on their prevention, particularly with regard to indirect complications, such as compressive neuropathies. It will be necessary to maintain the follow-up of these patients to understand the evolution of the neurological consequences associated with COVID-19.

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