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100 Cases By Conrad Fischer.pdfl

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100 Cases By Conrad Fischer.pdfl


MFS and GBS are thought to result from an aberrant acute autoimmune response to a preceding infection (e.g., Campylobacter jejuni, Cytomegalovirus, Epstein-Barr virus, or human immunodeficiency virus (HIV). A cross-reaction between peripheral nerve antigens and microbial/viral components through molecular mimicry is thought to drive the inflammatory process of this illness. [9][10][11] Approximately two-thirds of cases are preceded by symptoms of upper respiratory tract infection or diarrhea, and about 50% develop following an infection. Researchers do not fully understand the precise mechanism of pathogenesis. The immune response can be directed toward the myelin or the axon of the peripheral nerve.[12][7]

MFS is associated mainly with dysfunction of the third, fourth, and sixth cranial nerves. Documented cases have been reported, however, for most of the other cranial nerves. Antibodies against the GQ1b ganglioside are a typical serological finding as described in the pathophysiology section of this article, but the absence of antibodies does not rule out the disease completely. Other risk factors associated with the disease include the use of certain drugs (heroin, suramin, streptokinase, and isotretinoin), use of TNF-alpha antagonist therapy, other concurrent autoimmune diseases (systemic lupus, Hodgkin disease, and sarcoidosis), surgery, epidural anesthesia, bone marrow transplant, and immunizations. [13][14][15][8][16]

The worldwide incidence of GBS is approximately 1 to 2 in 100,000, with the MFS variant representing a tiny subset of the cases (1 to 2 in 1,000,000). It affects more men than women with an approximate gender ratio of 2:1 and a mean age of 43.6 years at the onset of disease.[17] It has a higher incidence in Asians, estimated between 15% to 25% of GBS in this population compared to 5% in the Western populations. A viral infection precedes the neurological symptoms in 72% of cases, with an average latent asymptomatic and incubation period of 10 days. A recent study that looked at patients admitted with GBS, MFS, and Bickerstaff brainstem encephalitis (BBE) in a tertiary hospital showed that recurrence of symptoms occurs at a higher rate in patients with MFS, and BBE, than GBS. [18] [19]

MFS is mainly treated with adequate supportive care, pain control, respiratory support as needed, and immunotherapy. Although used in the past, oral or intravenous (IV) steroids are no longer recommended in the treatment of GBS or MFS because they are ineffective. Corticosteroids may slow recovery from GBS they are recommended only in the setting of neuropathic or radicular pain. IV immunoglobulin (IVIg) and plasma exchange are both effective treatments for GBS and severe cases of MFS. No difference exists between the primary outcomes of mortality, disability, and length of intubation between IVIG and plasmapheresis. Patients with MFS usually do not require immunotherapy, presumably because they have a good prognosis and spontaneous recovery. IVIG should be considered in patients with severe Miller Fisher syndrome who have swallowing and respiratory difficulties, despite lack of supporting evidence of benefit. Overall, IVIG is preferred over exchange due to convenience, availability, and minimal adverse effects, however; the cost can be prohibitive for some low income or underinsured patients.[39][40][41] [42] [43] [44]

Neurology and possibly neuromuscular subspecialty consultations, if possible, should be considered for GBS or MFS cases. If needed, a critical care intensivist may need to be consulted for ICU admission and management.

The diagnosis and management of MFS are complex and best done with an interprofessional team that includes the neurologist, internist, intensivist, pulmonologist, physical therapist, ophthalmologist, psychiatrist, infectious disease expert, and ICU nurses. MFS is mainly treated with adequate supportive care, pain control, and respiratory support as needed, and immunotherapy. IVIG or plasmapheresis are the mainstays of therapy. Corticosteroids are no longer recommended and are ineffective in the majority of cases. Most patients require a prolonged stay in the hospital. The prognosis of MFS is usually good with a case fatality of less than 5%. The mean recovery times range from 8 to 12 weeks. Although recurrence may occur, it is uncommon.

Three recent cases illustrate the potential of lipid therapy in calcium channel blocker overdose. Young et al. present a case of multidrug overdose including 13.44 g of verapamil in combination with bupropion, zolpidem, quetiapine, clonazepam and benazepril [26]. Their patient presented to the hospital hypotensive and acidotic, requiring mechanical ventilation and norepinephrine to maintain arterial pressure. Lipid therapy was initiated almost immediately upon arrival, and within an hour the norepinephrine dose was halved. The patient was extubated on day two, and discharged on day five with no neurologic deficits. Montiel et al. describe a second case of a patient who ingested 3.6 g of sustained-release diltiazem who was treated with hyperinsulinemic euglycemia therapy in combination with lipid therapy [27]. Their patient had an improvement in blood pressure within one hour of beginning intravenous lipid, and was discharged from the intensive care unit on day nine with a full recovery. Finally, French et al. report a case of sustained verapamil overdose treated with lipid emulsion therapy. Notably, the serum level of verapamil in their case was slightly decreased after administration of lipids [28].

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