MUSEUM DUNIA MAYA DR IWAN S.
Dr IWAN ‘S CYBERMUSEUM
THE FIRST INDONESIAN CYBERMUSEUM
MUSEUM DUNIA MAYA PERTAMA DI INDONESIA
DALAM PROSES UNTUK MENDAPATKAN SERTIFIKAT MURI
PENDIRI DAN PENEMU IDE
Dr IWAN SUWANDY, MHA
The Driwan’s Cybermuseum
Andy Griffith receiving the Presidential Medal of Freedom.
|Born||Andy Samuel Griffith
June 1, 1926 (1926-06-01) (age 85)
Mount Airy, North Carolina, United States
|Education||Mount Airy High School|
|Alma mater||University of North Carolina at Chapel Hill|
|Occupation||Actor, comedian, director, producer, singer (country, bluegrass & southern gospel), writer|
|Notable works||The Andy Griffith Show|
|Spouse||Barbara Bray Edwards (m. 1949–72) (divorced)
Solica Cassuto (m. 1975–81) (divorced)
Cindi Knight (1983–present)American actor Andy Griffith developed Guillain-Barré syndrome in 1983
Andy Samuel Griffith (born June 1, 1926) is an American actor, director, producer, Grammy Award-winning Southern-gospel singer, and writer. He gained prominence in the starring role in director Elia Kazan‘s epic film A Face in the Crowd (1957) before he became better known for his television roles, playing the lead characters in the 1960–68 situation comedy, The Andy Griffith Show, and in the 1986–95 legal drama, Matlock. Griffith was awarded the Presidential Medal of Freedom by US President George W. Bush on November 9, 2005.
|Classification and external resources|
|eMedicine||emerg/222 neuro/7 pmr/48 neuro/598|
Guillain–Barré syndrome (GBS) (French pronunciation: [ɡiˈlɛ̃ baˈʁe], English pronunciation: /ˈɡiːlænˈbɑreɪ/), sometimes called Landry’s paralysis, is an acute inflammatory demyelinating polyneuropathy (AIDP), a disorder affecting the peripheral nervous system. Ascending paralysis, weakness beginning in the feet and hands and migrating towards the trunk, is the most typical symptom. It can cause life-threatening complications, particularly if the breathing muscles are affected or if there is dysfunction of the autonomic nervous system. The disease is usually triggered by an acute infection. Guillain–Barré syndrome is a form of peripheral neuropathy.
The diagnosis is usually made by nerve conduction studies. With prompt treatment by intravenous immunoglobulins or plasmapheresis, together with supportive care, the majority will recover completely. Guillain–Barré syndrome is rare, at 1–2 cases per 100,000 people annually, but is one of the leading causes of acute non-trauma-related paralysis in the world. The syndrome is named after the French physicians Georges Guillain and Jean Alexandre Barré, who described it in 1916.
Guillain Barré Syndrome Support Group Trust
Welcome to the website of the Guillain Barré (pronounced gee-lane bah-ray) Syndrome Support Group New Zealand Trust.
Guillain Barré syndrome was discovered by the French physicians Jean-Alexandre Barré, Georges Guillain and Andre Strohl in the early 1900s following tests on soldiers returning from World War 1. Many cases of an identical condition had been described over the preceding 80 years but these neurologists identified one of the characterising features of the disease – the increased concentration of protein in the spinal fluid without evidence of inflammation.
GBS is a polyneuritis (an inflammation of many nerves) that affects the peripheral nerves connecting the skin and muscles to the central nervous system and leads to progressive weakness in the arms and legs. It is caused by the body’s own immune system turning on itself and attacking the nerves by mistake
Guillain-Barré syndrome (GBS) (pengucapan Prancis: [ɡilɛ baʁe], pengucapan bahasa Inggris: / ɡi lænbɑreɪ ː /), kadang-kadang disebut kelumpuhan Landry, adalah suatu polineuropati demielinasi inflamasi akut (AIDP), gangguan yang mempengaruhi sistem saraf perifer. Ascending kelumpuhan, kelemahan awal pada kaki dan tangan dan bermigrasi ke bagasi, adalah gejala paling khas. Hal ini dapat menyebabkan komplikasi yang mengancam jiwa, terutama jika otot-otot pernapasan dipengaruhi atau jika ada disfungsi dari sistem saraf otonom. Penyakit ini biasanya dipicu oleh infeksi akut. Guillain-Barré syndrome adalah bentuk neuropati perifer.
Diagnosis biasanya dibuat dengan studi konduksi saraf. Dengan pengobatan prompt dengan imunoglobulin intravena atau plasmapheresis, bersama-sama dengan perawatan suportif, mayoritas akan sembuh sepenuhnya. Sindrom Guillain-Barré jarang, pada 1-2 kasus per 100.000 orang per tahun, namun merupakan salah satu penyebab utama akut non-trauma yang berhubungan dengan kelumpuhan di dunia.
Sindrom ini dinamai setelah Georges Guillain dan Jean dokter Alexandre Barre dari Perancis , yang digambarkan pada tahun 1916
contoh kasus di Indonesia
Askes Tanggung Biaya Pengobatan Penderita GBS
Six different subtypes of Guillain–Barré syndrome exist:
- Acute inflammatory demyelinating polyneuropathy (AIDP) is the most common form of GBS, and the term is often used synonymously with GBS. It is caused by an auto-immune response directed against Schwann cell membranes.
- Miller Fisher syndrome (MFS) is a rare variant of GBS and manifests as a descending paralysis, proceeding in the reverse order of the more common form of GBS. It usually affects the eye muscles first and presents with the triad of ophthalmoplegia, ataxia, and areflexia. Anti-GQ1b antibodies are present in 90% of cases.
- Acute motor axonal neuropathy (AMAN), also known as Chinese paralytic syndrome, attacks motor nodes of Ranvier and is prevalent in China and Mexico. It is probably due to an auto-immune response directed against the axoplasm of peripheral nerves. The disease may be seasonal and recovery can be rapid. Anti-GD1a antibodies are present. Anti-GD3 antibodies are found more frequently in AMAN.
- Acute motor sensory axonal neuropathy (AMSAN) is similar to AMAN but also affects sensory nerves with severe axonal damage. Like AMAN, it is probably due to an auto-immune response directed against the axoplasm of peripheral nerves. Recovery is slow and often incomplete.
- Acute panautonomic neuropathy is the most rare variant of GBS, sometimes accompanied by encephalopathy. It is associated with a high mortality rate, owing to cardiovascular involvement, and associated dysrhythmias. Impaired sweating, lack of tear formation, photophobia, dryness of nasal and oral mucosa, itching and peeling of skin, nausea, dysphagia, constipation unrelieved by laxatives or alternating with diarrhea occur frequently in this patient group. Initial nonspecific symptoms of lethargy, fatigue, headache, and decreased initiative are followed by autonomic symptoms including orthostatic lightheadedness, blurring of vision, abdominal pain, diarrhea, dryness of eyes, and disturbed micturition. The most common symptoms at onset are related to orthostatic intolerance, as well as gastrointestinal and sudomotor dysfunction (Suarez et al. 1994). Parasympathetic impairment (abdominal pain, vomiting, constipation, ileus, urinary retention, dilated unreactive pupils, loss of accommodation) may also be observed.
- Bickerstaff’s brainstem encephalitis (BBE), is a further variant of Guillain–Barré syndrome. It is characterized by acute onset of ophthalmoplegia, ataxia, disturbance of consciousness, hyperreflexia or Babinski’s sign. The course of the disease can be monophasic or remitting-relapsing. Large, irregular hyperintense lesions located mainly in the brainstem, especially in the pons, midbrain and medulla are described in the literature. BBE despite severe initial presentation usually has a good prognosis. Magnetic resonance imaging (MRI) plays a critical role in the diagnosis of BBE. A considerable number of BBE patients have associated axonal Guillain–Barré syndrome, indicative that the two disorders are closely related and form a continuous spectrum.
Signs and symptoms
The disorder is characterized by symmetrical weakness which usually affects the lower limbs first, and rapidly progresses in an ascending fashion. Patients generally notice weakness in their legs, manifesting as “rubbery legs” or legs that tend to buckle, with or without dysesthesias (numbness or tingling). As the weakness progresses upward, usually over periods of hours to days, the arms and facial muscles also become affected. Frequently, the lower cranial nerves may be affected, leading to bulbar weakness, oropharyngeal dysphagia (drooling, or difficulty swallowing and/or maintaining an open airway) and respiratory difficulties. Most patients require hospitalization and about 30% require ventilatory assistance for treatment of Type II respiratory failure.  Facial weakness is also commonly a feature, but eye movement abnormalities are not commonly seen in ascending GBS, but are a prominent feature in the Miller-Fisher variant (see below.) Sensory loss, if present, usually takes the form of loss of proprioception (position sense) and areflexia (complete loss of deep tendon reflexes), an important feature of GBS. Loss of pain and temperature sensation is usually mild. In fact, pain is a common symptom in GBS, presenting as deep aching pain, usually in the weakened muscles, which patients compare to the pain from overexercising. These pains are self-limited and should be treated with standard analgesics. Bladder dysfunction may occur in severe cases but should be transient. If severe, spinal cord disorder should be suspected.
Fever should not be present, and if it is, another cause should be suspected.
Acute paralysis in Guillain–Barré syndrome may be related to sodium channel blocking factor in the cerebrospinal fluid (CSF). Significant issues involving intravenous salt and water administration may occur unpredictably in this patient group, resulting in SIADH. SIADH is one of the causes of hyponatremia and can be accompanied with various conditions such as malignancies, infections and nervous system diseases. Symptoms of Guillain-Barré syndrome such as general weakness, decreased consciousness, and seizure are similar to those of hyponatremia
Tanda dan gejala
Kelainan ini ditandai oleh kelemahan simetris yang biasanya mempengaruhi tungkai bawah pertama, dan dengan cepat berkembang dalam mode menaik. Pasien umumnya menyadari kelemahan di kaki mereka, mewujudkan sebagai “kaki karet” atau kaki yang cenderung gesper, dengan atau tanpa dysesthesias (mati rasa atau kesemutan). Sebagai kelemahan berlangsung ke atas, biasanya selama periode jam untuk hari, lengan dan otot-otot wajah juga menjadi terpengaruh. Sering, saraf kranial yang lebih rendah mungkin akan terpengaruh, menyebabkan kelemahan bulbar, disfagia orofaringeal (air liur, atau kesulitan menelan dan / atau mempertahankan jalan napas terbuka) dan kesulitan pernafasan. Kebanyakan pasien memerlukan rawat inap dan sekitar 30% memerlukan bantuan ventilasi untuk pengobatan kegagalan pernafasan Tipe II  . Kelemahan wajah juga sering fitur, tapi mata kelainan gerakan yang tidak biasa terlihat dalam ascending GBS, tetapi fitur yang menonjol di varian Miller-Fisher (lihat di bawah.) kehilangan sensorik, jika ada, biasanya mengambil bentuk hilangnya proprioception (rasa posisi) dan areflexia (hilangnya lengkap refleks tendon dalam), sebuah fitur penting dari GBS. Hilangnya sensasi nyeri dan suhu biasanya ringan. Bahkan, nyeri adalah gejala yang umum di GBS, menyajikan sebagai nyeri yang dalam, biasanya pada otot melemah, yang pasien dibandingkan dengan rasa sakit dari overexercising. Rasa sakit adalah diri terbatas dan harus diobati dengan analgesik standar. Disfungsi kandung kemih dapat terjadi pada kasus yang berat tetapi harus sementara. Jika parah, gangguan sumsum tulang belakang harus dicurigai.
Demam tidak harus hadir, dan jika itu, penyebab lain harus dicurigai.
Dalam kasus yang parah GBS, hilangnya fungsi otonom adalah umum, mewujudkan sebagai fluktuasi luas dalam tekanan darah, hipotensi ortostatik, dan aritmia jantung.
Kelumpuhan akut pada sindrom Guillain-Barré mungkin berkaitan dengan saluran natrium memblokir faktor dalam cairan cerebrospinal (CSF). Isu-isu signifikan yang melibatkan garam intravena dan administrasi air dapat terjadi tak terduga pada kelompok pasien ini, sehingga SIADH. SIADH adalah salah satu penyebab hiponatremia dan dapat disertai dengan berbagai kondisi seperti keganasan, infeksi dan penyakit sistem saraf. Gejala sindrom Guillain-Barré seperti kelemahan umum, penurunan kesadaran, dan kejang yang mirip dengan hiponatremia
Gejala-gejala sindrom Guillain-Barré juga mirip dengan yang untuk neuropati inflamasi progresif
All forms of Guillain–Barré syndrome are due to an immune response to foreign antigens (such as infectious agents) that is mistargeted at host nerve tissues instead. The targets of such immune attack are thought to be gangliosides, compounds naturally present in large quantities in human nerve tissues. The most common antecedent infection is the bacterium Campylobacter jejuni. However, 60% of cases do not have a known cause. One study suggests that a minority of cases may be triggered by the influenza virus, or by an immune reaction to the influenza virus.
The end result of such autoimmune attack on the peripheral nerves is damage to the myelin, the fatty insulating layer of the nerve, and a nerve conduction block, leading to a muscle paralysis that may be accompanied by sensory or autonomic disturbances.
However, in mild cases, nerve axon (the long slender conducting portion of a nerve) function remains intact and recovery can be rapid if remyelination occurs. In severe cases, axonal damage occurs, and recovery depends on the regeneration of this important tissue. Recent studies on the disorder have demonstrated that approximately 80% of the patients have myelin loss, whereas, in the remaining 20%, the pathologic hallmark of the disorder is indeed axon loss.
Becoming infected with influenza increases both the risk of developing GBS and the risk of death (up to 1 in 10,000 who get influenza will die from it). While influenza vaccines have sometimes been suspected to raise the incidence of GBS, the evidence is equivocal, as shown below. Moreover, the highest level of suspected risks from the influenza vaccine is less than one-tenth the risk from the influenza disease itself, as discussed in more detail in the next section.
GBS may be a rare side-effect of influenza vaccines; a study of the Vaccine Adverse Event Reporting System (VAERS) indicates that it is reported as an adverse event potentially associated with the vaccine at a rate of 1 per million vaccines (over the normal risk). There were reports of GBS affecting 10 per million who had received swine flu immunizations in the 1976 U.S. outbreak of swine flu—25 of which resulted in death from severe pulmonary complications, leading the United States Center of Disease Control to end that immunization campaign within the United States. (By comparison, the average flu season kills around 30,000 people in the United States). However, the role of the vaccine even in those 25 cases in 1976 has remained unclear, partly because GBS had an unknown but very low incidence rate in the general population making it difficult to assess whether the vaccine was really increasing the risk for GBS. Later research has pointed to the absence of, or only a very small increase in, the GBS risk due to the 1976 swine flu vaccine. Furthermore, the GBS may not have been directly due to the vaccine but to a bacterial contamination of the 1976 vaccine.
From October 6 to November 24, 2009, the U.S. CDC, through the VAERS reporting system, received ten reports of Guillain-Barré syndrome cases associated with the H1N1 vaccine and identified two additional probable cases from VAERS reports (46.2 million doses were distributed within the U.S. during this time). Only four cases, however, meet the Brighton Collaboration case criteria for Guillain–Barré syndrome, while four do not meet the criteria and four remain under review. A preliminary report by the CDC‘s Emerging Infections Programs (EIP) calculates the rate of GBS observed in patients who previously received the 2009 H1N1 influenza vaccination is an excess of 0.8 per million cases, which is on par with the rate seen with the seasonal trivalent influenza vaccine.
Although one review gives an incidence of about one case per million vaccinations, a large study in China, reported in the NEJM covering close to 100 million doses of vaccine against the 2009 H1N1 “swine” flu found only eleven cases of Guillain-Barré syndrome (0.1%) total incidence in persons vaccinated, actually lower than the normal rate of the disease in China, and no other notable side effects; “The risk-benefit ratio, which is what vaccines and everything in medicine is about, is overwhelmingly in favor of vaccination.”
The diagnosis of GBS usually depends on findings such as rapid development of muscle paralysis, areflexia, absence of fever, and a likely inciting event. Cerebrospinal fluid analysis (through a lumbar spinal puncture) and electrodiagnostic tests of nerves and muscles (such as nerve conduction studies) are common tests ordered in the diagnosis of GBS.
- Typical CSF findings include albumino-cytological dissociation. As opposed to infectious causes, this is an elevated protein level (100–1000 mg/dL), without an accompanying increased cell count pleocytosis. A sustained increased white blood cell count may indicate an alternative diagnosis such as infection.
- Electromyography (EMG) and nerve conduction study (NCS) may show prolonged distal latencies, conduction slowing, conduction block, and temporal dispersion of compound action potential in demyelinating cases. In primary axonal damage, the findings include reduced amplitude of the action potentials without conduction slowing.
- Progressive, relatively symmetrical weakness of two or more limbs due to neuropathy
- Disorder course < 4 weeks
- Exclusion of other causes (see below)
- relatively symmetric weakness accompanied by numbness and/or tingling
- mild sensory involvement
- facial nerve or other cranial nerve involvement
- absence of fever
- typical CSF findings obtained from lumbar puncture
- electrophysiologic evidence of demyelination from electromyogram
- acute myelopathies with chronic back pain and sphincter dysfunction
- botulism with early loss of pupillary reactivity and descending paralysis
- diphtheria with early oropharyngeal dysfunction
- Lyme disease polyradiculitis and other tick-borne paralyses
- porphyria with abdominal pain, seizures, psychosis
- vasculitis neuropathy
- poliomyelitis with fever and meningeal signs
- CMV polyradiculitis in immunocompromised patients
- critical illness neuropathy
- myasthenia gravis
- poisonings with organophosphate, poison hemlock, thallium, or arsenic
- intoxication with Karwinskia humboldtiana leaves or seeds
- paresis caused by West Nile virus
- spinal astrocytoma
- motor neurone disease
- West Nile virus can cause severe, potentially fatal neurological illnesses, which include encephalitis, meningitis, Guillain-Barré syndrome, and anterior myelitis.
Supportive care with monitoring of all vital functions is the cornerstone of successful management in the acute patient. Of greatest concern is respiratory failure due to paralysis of the diaphragm. Early intubation should be considered in any patient with a vital capacity (VC) <20 ml/kg, a negative inspiratory force (NIF) that is less negative (i.e., closer to zero) than -25 cmH2O, more than 30% decrease in either VC or NIF within 24 hours, rapid progression of disorder, or autonomic instability.
Once the patient is stabilized, treatment of the underlying condition should be initiated as soon as possible. Either high-dose intravenous immunoglobulins (IVIg) at 400 mg/kg for 5 days or plasmapheresis can be administered, as they are equally effective and a combination of the two is not significantly better than either alone. Therapy is no longer effective two weeks after the first motor symptoms appear, so treatment should be instituted as soon as possible. IVIg is usually used first because of its ease of administration and safety profile, with a total of five daily infusions for a total dose of 2 g/kg body weight (400 mg/kg each day). The use of intravenous immunoglobulins is not without risk, occasionally causing hepatitis, or in rare cases, renal failure if used for longer than five days. Glucocorticoids have not been found to be effective in GBS. If plasmapheresis is chosen, a dose of 40-50 mL/kg plasma exchange (PE) can be administered four times over a week.
Following the acute phase, the patient may also need rehabilitation to regain lost functions. This treatment will focus on improving ADL (activities of daily living) functions such as brushing teeth, washing, and getting dressed. Depending on the local structuring on health care, a team of different therapists and nurses will be established according to patient needs. An occupational therapist can offer equipment (such as wheelchair and special cutlery) to help the patient achieve ADL independence. A physiotherapist would plan a progressive training program and guide the patient to correct functional movement, avoiding harmful compensations which might have a negative effect in the long run. There is also some evidence supporting physiotherapy in helping patients with Guillain–Barré syndrome regain strength, endurance, and gait quality, as well as helping them prevent contractures, bedsores, and cardiopulmonary difficulties. A speech and language therapist would be essential in the patient regaining speaking and swallowing ability if they were intubated and received a tracheostomy. The speech and language therapist would also offer advice to the medical team regarding the swallowing abilities of the patient and would help the patient regain their communication ability pre-dysarthria. There would also be a doctor, nurse and other team members involved, depending on the needs of the patient. This team contribute their knowledge to guide the patient towards his or her goals, and it is important that all goals set by the separate team members are relevant for the patient’s own priorities. After rehabilitation the patient should be able to function in his or her own home and attend necessary training as needed.
Most of the time recovery starts after the fourth week from the onset of the disorder. Approximately 80% of patients have a complete recovery within a few months to a year, although minor findings may persist, such as areflexia. About 5–10% recover with severe disability, with most of such cases involving severe proximal motor and sensory axonal damage with inability of axonal regeneration. However, this is a grave disorder and despite all improvements in treatment and supportive care, the death rate among patients with this disorder is still about 2–3% even in the best intensive care units. Worldwide, the death rate runs slightly higher (4%), mostly from a lack of availability of life support equipment during the lengthy plateau lasting four to six weeks, and in some cases up to one year, when a ventilator is needed in the worst cases. About 5–10% of patients have one or more late relapses, in which case they are then classified as having chronic inflammatory demyelinating polyneuropathy (CIDP).
Poor prognostic factors include: 1) age, over 40 years, 2) history of preceding diarrheal illness, 3) requiring ventilator support, 4) high anti-GM1 titre and 5) poor upper limb muscle strength.
The incidence of GBS during pregnancy is 1.7 cases per 100,000 of the population. The mother will generally improve with treatment but death of the fetus is a risk. The risk of Guillain–Barré syndrome increases after delivery, particularly during the first two weeks postpartum. There is evidence of Campylobacter jejuni as an antecedent infection in approximately 26% of disease cases, requiring special care in the preparation and handling of food. Congenital and neonatal Guillain–Barré syndrome have also been reported.
The disorder was first described by the French physician Jean Landry in 1859. In 1916, Georges Guillain, Jean Alexandre Barré, and André Strohl diagnosed two soldiers with the illness and discovered the key diagnostic abnormality of increased spinal fluid protein production, but normal cell count.
GBS is also known as acute idiopathic polyradiculoneuritis, acute idiopathic polyneuritis, French polio, Landry’s ascending paralysis and Landry Guillain Barré syndrome.
American actor Andy Griffith developed Guillain-Barré syndrome in 1983. Griffith is seen here receiving an award at the White House in 2005
- Markus Babbel, former international footballer, contracted GBS in 2001, following a period suffering from the Epstein–Barr virus. He lost almost an entire year of his footballing career between the two illnesses and never again demonstrated the same level of ability that won him over 50 caps for Germany.
- Tony Benn, British politician.
- Rachel Chagall, actress, contracted GBS in 1982. In 1987 she portrayed Gabriela Brimmer, a notable disabilities activist.
- Samuel Goldstein, American athlete and Paralympian
- Andy Griffith, American actor on Andy Griffith Show, and Matlock. He developed Guillain–Barré in 1983.
- Joseph Heller, author, contracted GBS in 1981. This episode in his life is recounted in the autobiographical No Laughing Matter, which contains alternating chapters by Heller and his good friend Speed Vogel.
- Luci Baines Johnson, daughter of President Lyndon Johnson and Lady Bird Johnson. Diagnosed and under treatment for Guillain–Barré in April 2010.
- Hugh McElhenny, former Hall-of-Fame, professional American football player with the San Francisco 49ers.
- Lucky Oceans, Grammy Award winning musician with Asleep at the Wheel was diagnosed with GBS in 2008.
- Len Pasquarelli, sports writer and analyst for ESPN and resident of the Pro Football Writers of America, diagnosed in 2008.
- Serge Payer, Canadian-born professional hockey player. After battling and overcoming the syndrome, he set up the Serge Payer Foundation, which is dedicated to raising money for research into new treatments and cures for Guillain–Barré syndrome.
- William “The Refrigerator” Perry, former professional American football player with the Chicago Bears was diagnosed with GBS in 2008.
- Franklin D. Roosevelt, U.S. president. In 2003, a peer-reviewed study  found that Roosevelt’s paralysis—long attributed to poliomyelitis—was more likely caused by Guillain–Barré syndrome.
- Norton Simon, American industrialist and philanthropist.
- Hans Vonk, Dutch conductor.
- Danny Wuerffel, 1996 Heisman Trophy winner from the University of Florida
- case report from Indonesia(l0is,2011)
Case Report From Indonesia (Lois)
In 1982 my younger sister suddenly paralyzed after a few days before experiencing pain colds / flu-like. The beginning of a limp leg and quickly loose all over his body, but does not affect the face, the power of memory and can speak normally. The doctor said the pain is GBS as contained in this post. Time was already seeing where where in Indonesia and also to China, but my sister still remains paralyzed from the waist down.
While my brother was not able to walk and uses a wheelchair, he can run the business legacy of our parents’ shop. Hopefully those who also suffer from GBS disease now can get the treatment that is more up to date …. until the paralysis is not permanent
Laporan Kasus Dari indonesia(Lois)
Tahun 1982 adik perempuan saya tiba tiba lumpuh setelah beberapa hari sebelumnya mengalami sakit masuk angin/seperti flu. Permulaan kaki yang lemas dan dengan cepat lemas sekujur badan, tapi tidak mempengaruhi wajah, daya ingatan dan bisa berbicara normal. Kata dokter sakitnya adalah GBS seperti yang termuat dalam posting ini. Waktu itu udah berobat kemana mana di Indonesia dan juga sampai ke China, tapi adik saya sampai sekarang masih tetap lumpuh dari pinggang kebawah.
Walau adik saya itu tidak bisa jalan dan menggunakan kursi roda, dia bisa menjalankan usaha toko peninggalan orang tua kami. Semoga mereka yang juga menderita penyakit GBS sekarang ini bisa mendapatkan pengobatan yang lebih up to date…. hingga kelumpuhan tidak bersifat permanen
COPYRIGHT @ Dr IWAN SUWANDY 2011