We reported a rare case demonstrating that the hyperbaric oxygen chamber provided faster clinical improvement in a patient with a variant of Guillain-Barre Syndrome (GBS). A patient with progressive, acute weakness of upper extremity locomotor muscles and with difficulty breathing and swallowing was diagnosed with axonal GBS. Despite life-saving conventional therapies, there was no significant improvement until day 5. During hyperbaric oxygen therapy, there were daily gradual improvements until day 20, at which time the patient was capable of walking slowly without using a walking aid.
Objectives. Acute motor axonal neuropathy (AMAN) is a disease that leads to acute flaccid paralysis and may result from the binding of antibody and antigen to the spinal cord. The objective of this study is to evaluate the protective effect of hyperbaric oxygen treatment (HBOT) on axon degeneration of the spinal cord and sciatic nerve of the AMAN model rabbit. Axonal degeneration was assessed by evaluating glutathione (GSH) activity, interleukin-1β (IL-1β) expression, and clinical and histopathological features. Methods. Twenty-one New Zealand rabbits were divided into three groups. The treatment group was exposed to 100% oxygen at 2.4 ATA 90 minutes for 10 days at a decompression rate of 2.9 pounds per square inch/minute. GSH level was evaluated using an enzyme-linked immune-sorbent assay. An expression of IL-1β in the spinal cord was determined by immunohistochemistry. Clinical appearances were done by motor scale and body weight. Histological features observed neuronal swelling and inflammatory infiltration in the sagittal lumbar region and the undulation of the longitudinal sciatic nerve. Results. Rabbits exposed to HBO had high GSH activity levels ( p < 0.05 ) but unexpectedly had high IL1β expression ( p > 0.05 ). In addition, the HBO-exposed rabbits had a better degree of undulation, the size of neuronal swelling was smaller, the number of macrophages was higher, and motor function was better than the AMAN model rabbits ( p < 0.05 ). Conclusions. These findings indicate that HBO therapy can decrease axon degeneration by triggering GSH activity, increasing IL-1β level, and restoring tissues and motor status. In conclusion, HBO has a protective effect on axon degeneration of the spinal cord and sciatic nerve of the AMAN model rabbit.
Acute motor axonal neuropathy (AMAN) is a rare immune-mediated disorder characterized by acute flaccid paralysis with elevated levels of GM1 antibodies. It is also known as a subtype of the Guillain-Barre syndrome (GBS) and develops since antigen s serve as antibodies in the spinal cord. We report a case diagnosed as AMAN with symptoms of ascending limb symmetrical weakness. A neurological examination revealed a flaccid paralysis with multiple cranial nerve palsies. Electromyography showed an axonal type of GBS. The patient refused bone marrow fluid aspiration. Intravenous immunoglobulin was administered at the high care unit. Unfortunately, despite the standard therapy, an optimal recovery was not obtained. Hyperbaric oxygen (HBO) therapy has been known to be common in illnesses and some clinical diseases. Although it has not been indicated for peripheral neuropathy, a remarkable recovery was soon visible in the HBO-treated AMAN case. The HBO mechanisms involved here are anti-inflammation and immunomodulation.
BACKGROUND: Guillain-Barre syndrome (GBS) is considered an acute immune-mediated monophasic illness. Standard therapy includes intravenous immunoglobulin (IVIG) and/or plasmapheresis. Yet, long-standing disability remains a problem. In Indonesia, the availability and cost of these therapies are constraints. AIM: To show the capability of hyperbaric oxygen (HBO2) therapy in GBS patients who did not undergo standard therapy. HBO2 also provides healing in patients who experience delays in therapy. METHODS: Data included identity, demographic, social history, current disease history, disease progression and therapies used. Data were displayed in the form of tables and graphs. RESULTS: Twenty-five GBS patients underwent HBO2 from 2016 to 2019. The majority of patients were males aged 20-30 years, triggered by preceding diarrhea. After approximately three to ten days following HBO2, they felt their first positive changes. They walked with assistance after two to three weeks receiving HBO2 and without assistance after four to 12 weeks receiving HBO2. CONCLUSION: HBO2 administration show clinical improvement in GBS patients. HBO2 is expected to become an adjuctive therapy for GBS patients in Indonesia.
BACKGROUND: Acute motor axonal neuropathy (AMAN) is a peripheral nerve disorder that attacks motor axons and occurs acutely. AMAN is one type of Guillain–Barre syndrome (GBS) which often attacks men of productive age. Until now, although patients have undergone intravenous immunoglobulin (IVIG) therapy and/or plasmapheresis, long-standing disability remains a problem. In Indonesia, the availability and cost of these therapies are constraints. AIM: Our study aimed to find a proper animal model suitable for AMAN and can be executed in our institution, Naval Health Institute with a hope to find new therapeutic modalities in healing with AMAN. METHODS: GM1 ganglioside immunized in New Zealand male white rabbits with complete Freund’s adjuvant, every 3 weeks until 20 weeks. We evaluated the effects GM1 ganglioside on body weight, functional score, and axon degeneration’s scale. Functional score was examined based on Tarlov’s. Hematoxylin-eosin was used to stain this slide. RESULTS: Rabbits that being immunized with GM1 ganglioside experience a number of neurological signs and symptoms that resemble AMAN, that is, sluggish righting reflex, muscular weakness, flaccid hyper paralysis, and body weight loss. Pathological examination shows extensive degeneration of peripheral nerves, infiltration of macrophages, and perineuritis. CONCLUSION: This histological and clinical findings support that this neuropathy is induced by an autoimmune response delivered by cells that respond to gangliosides.
ABSTRAK Latar Belakang: Secara klinis, leukostasis didiagnosa pada pasien leukemia dengan hasil laboratorium hiperleukositosis (>100.000 u/L) disertai manifestasi respiratorik, neurologis, atau renal. Insidensi hiperleukositosis pada Leukemia Limfoblastik Akut (LLA) usia dewasa 10-30%, jarang pada wanita, dan jarang menyebabkan leukostasis. Laporan Kasus: Seorang wanita berusia 20 tahun dikonsulkan dari bagian penyakit dalam dengan kejang umum tonik-klonik. Hasil laboratorium menunjukkan leukosit 134.500 u/L, hasil EKG menunjukkan iskemik miokardium. Diskusi: Leukostasis jarang terjadi pada pasien leukemia. Leukostasis menyebabkan aliran oksigen dalam darah menuju sel menjadi inadekuat, termasuk salah satunya aliran darah yang menuju sel otak. Hipoksia jaringan otak merupakan salah satu faktor pemicu terjadinya kejang. Kesimpulan: Leukostasis merupakan suatu keadaan emergensi yang dapat meningkatkan morbiditas dan mortalitas pasien. Tujuan tatalaksana penyakit adalah mengurangi mortalitas dini, termasuk tatalaksana kejang, yang merupakan salah satu menifestasi klinis leukostasis. Kata kunci: kejang, leukostasis, leukemia. ABSTRACT Background: Clinically, leukostasis is diagnosed in patients with leukemia with laboratory results of hyperleukocytosis (> 100,000 u / L) followed by respiratory, neurological, or renal manifestations. The incidence of hyperleukocytosis in Acute Lymphoblastic Leukemia (LLA) is 10-30% of adult age, rare in women, and rarely causes leukostasis. Case Report: A 20th-years-old woman was consulted from an Internal Medicine Department with a tonic-clonic general seizure. Laboratory results showed that leukocytes were 134,500 U / L and ECG results showed an ischemic myocardium. Discussion: Leukostasis rarely occurs in leukemic patients. Leukostasis causes the flow of oxygen in the blood to the cells to be inadequate, including the blood flow to brain cells. Brain tissue hypoxia is one of the trigger factors for seizures. Conclussion: Leukostasis is an emergency situation that can increase patient morbidity and mortality. The aim of disease management is to reduce early mortality, including management of seizures, which is one of the clinical manifestations of leukostasis. Keywords: seizure, leukostasis, leukemia.
In December 2019, coronavirus pandemic re-emerged. Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has been identified as the causation in series of acute pneumonia cases discovered in Wuhan in Hubei Province, China. This disease is officially named COVID-19 by WHO. Symptoms manifestation of COVID-19 range from fever, malaise, myalgia, headache, to respiratory system symptoms of cough, stuffy/runny nose, and difficulty breathing. In severe cases, it may result in ARDS. A case study has reported that COVID-19 may also have cardiovascular manifestation, i.e. life threatening arrhythmia. Although COVID-19 is a respiratory infection and cardiovascular event is the main cause of fatality, medical professionals must understand its neurological complications in order to reduce mortality rate in infected patients. Further researches on specific risk factors or determinant protective factors from the neurological symptoms are needed to reduce risk of complication in COVID-19 infection cases.
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