for those who r interested in medcine:what was the rare disease of president Roosevelt?

10 points goes to any who gives me the best answer, i know his medical condition , but i ask a question like this everyday about a celebrity who suffered a certain disease , to make u enjoy this dull sector.. lol enjoy urselves!
Answer:
Guillain-Barré syndrome Background: In 1859, Landry published a report on 10 patients with an ascending paralysis. This was followed by a report in 1916 written by 3 French physicians working in the Sixth Army camp during the First World War; they described 2 French soldiers with motor weakness, areflexia, and “albuniocytological dissociation” in the cerebrospinal fluid. In this report Guillain, Barré, and Strohl carefully recorded and interpreted the tendon reflexes of their patients and became the first to recognize the peripheral nature of the illness. Further cases were recognized, and the identified syndrome was later named Guillain-Barré syndrome (GBS). Historically, GBS was a single disorder; however, current practice divides the syndrome into several variant forms.GBS is a heterogeneous grouping of immune-mediated processes generally characterized by motor, sensory, and autonomic dysfunction. In its classic form, GBS is an acute inflammatory demyelinating polyneuropathy characterized by progressive symmetric ascending muscle weakness, paralysis, and hyporeflexia with or without sensory or autonomic symptoms; however, variants involving the cranial nerves or pure motor involvement are not uncommon. In severe cases, muscle weakness may lead to respiratory failure, and labile autonomic dysfunction may complicate the use of vasoactive and sedative drugs.Pathophysiology: Although the clinical syndrome classically presents as a rapidly progressive acute polyneuropathy, several pathologic and etiologically subtypes exist. Most patients with GBS exhibit absent or profoundly delayed conduction in action nerve fibers. This aberrant conduction results from demyelination of nerve cell axons. Peripheral nerves and spinal roots are the major sites of demyelination, but cranial nerves also may be involved.GBS is believed to result from an autoimmune response, both humoral and cell mediated, to a recent infection or any of a long list of medical problems. Its relation to antecedent infections and the identification of various antiganglioside antibodies suggest that molecular mimicry may serve as a possible mechanism for the disease. The antibodies formed against gangliosidelike epitopes in the lipopolysaccharide layer of some infectious agents have been shown in both necropsy and animal models to cross-react with the ganglioside surface molecules of peripheral nerves. Symptoms generally coincide pathologically with various patterns of lymphocytic infiltration and macrophage-mediated demyelination, depending on the subtype in question. Recovery is typically associated with remyelination. In a subset of patients, GBS is associated primarily with myelin-sparing axonal damage resulting from a direct cellular immune attack on the axon itself.The acute inflammatory demyelinating polyneuropathy (AIDP) subtype of GBS is by far the most commonly identified form in the United States. It is generally preceded by an antecedent bacterial or viral infection. Nearly 40% of patients are seropositive for Campylobacter jejuni. Lymphocytic infiltration and macrophage-mediated demyelination of the peripheral nerves are present. Symptoms generally resolve with remyelination.The acute motor axonal neuropathy (AMAN) subtype is a purely motor subtype, which is more prevalent amongst pediatric age groups. Nearly 70-75% of patients are seropositive for Campylobacter. One third of these cases may actually be hyperreflexic. AMAN is generally characterized by a rapidly progressive weakness, ensuing respiratory failure, and good recovery.Acute motor-sensory axonal neuropathy (AMSAN) is an acute severe illness similar to AMAN except that AMSAN also affects sensory nerves and roots. Patients are typically adults with both motor and sensory dysfunction, marked muscle wasting, and poor recovery.Miller-Fisher syndrome (MFS) is a rare variant that typically presents with the classic triad of ataxia, areflexia, and ophthalmoplegia. The ataxia tends to be out of proportion to the degree of sensory loss. Patients may also have mild limb weakness, ptosis, facial palsy, or bulbar palsy. Anti-GQ1b antibodies are prominent in this variant, and patients have reduced or absent sensory nerve action potentials and absent tibial H reflex. Recovery generally occurs within 1-3 months.Acute panautonomic neuropathy is among the rarest of all variants and involves both the sympathetic and parasympathetic nervous systems. Cardiovascular involvement is common, and dysrhythmias are a significant source of mortality in this form of the disease. The patient may also experience sensory symptoms. Recovery is gradual and often incomplete.

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POLIO! or GUILLAN-Barré syndrome Poliomyelitis, often called polio or infantile paralysis, is a virally induced infectious disease which spreads via the fecal-oral route. Franklin D. Roosevelt may have contracted polio in 1921. The unquestioned diagnosis at the time and thereafter in countless references was paralytic poliomyelitis. Yet his age (39 years) and many features of his illness are more consistent with a diagnosis of Guillain-Barré syndrome (an autoimmune peripheral neuropathy).After Franklin D. Roosevelt contracted polio, the disease took on a new image as Roosevelt's disease and helped recast the image of the cripple.

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depression

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Poliomyletis, if I've spelled it correctly, also known as infantile paralysis or polio. And it wasn't rare: both my parents suffered from it, though their cases were far less severe than Mr Roosevelt's. The disease was just about wiped out until some third-world witch doctors objected.

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Guillain-Barré syndromeGuillain-Barré syndrome (GBS) is an acute, autoimmune, polyradiculoneuropathy affecting the peripheral nervous system, usually triggered by an acute infectious process. There are several types of GBS, but unless otherwise stated, GBS refers to the most common form, acute inflammatory demyelinating polyneuropathy (AIDP). It is frequently severe and usually exhibits as an ascending paralysis noted by weakness in the legs that spreads to the upper limbs and the face along with complete loss of deep tendon reflexes. With prompt treatment with immunoglobulins and supportive care, majority of patients will regain full functional capacity. However, death may occur if severe pulmonary complications and dysautonomia are present.

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