Fdr 3

Anonymous
October 4, 2006 at 3:09 am

What happens next?
The worst degree of weakness is usually reached within four weeks and always within six weeks. Some patients deteriorate very rapidly to a state of severe paralysis over the course of a few days but this is uncommon. The patient then enters a plateau phase that usually lasts a few days or weeks during which the course of the disease seems stationary. Most people are so weak during this stage that they are confined to a hospital bed where rest is probably a good thing. However, it is very important to keep all the joints moving through a full range to stop them stiffening up. The physiotherapist is in charge of this physical therapy and will be pleased to advise relatives and friends on what they can do to help.
Symptoms
The severity of CIDP is extremely variable and the symptoms experienced vary considerably between patients. Initial symptoms may be vague and confusing to both the patient and the doctor. Subjective symptoms such as fatigue and sensory disturbance are difficult to communicate. In the early stages it may be difficult for the patient to persuade the doctor that there is anything physically wrong.
Early symptoms usually include either tingling (pins and needles) or loss of feeling (numbness) beginning in the toes and fingers, or weakness, so that legs feel heavy and wooden, arms feel limp and hands cannot grip or turn things properly. These symptoms may remain mild and result in only minor disruption the patient’s normal life. Alternatively they may become progressively and gradually worse over a period of several weeks, months or even years sometimes, but very rarely, to the extent that the patient is bed bound with profound weakness of the arms.
CIDP usually presents with both weakness and sensory symptoms, sometimes with weakness alone, and rarely with sensory symptoms alone. The arms and legs are usually affected together, the legs more than the arms. Prickling and tingling sensations in the extremities are common and may be painful. Aching pain in the muscles also occurs. Tendon reflexes are usually lost. As the disease becomes more severe, a tremor may develop, usually in the upper limbs. Very rarely patients may develop facial weakness.
Diagnosis
Health officials convinced the Chinese to rename the bulk of their polio to Guillaine Barre Syndrome (GBS). A study found that the new disorder (Chinese Paralytic syndrome) and the GBS was really polio (41). After mass vaccination in 1971, reports of polio went down but GBS increased about 10 fold.(Ref: Vaccination by Greg Beattie)
Tang XF, et al. Guillain-Barre syndrome or “new” Chinese paralytic syndrome in northern China? Electroencephalogr Clin Neurophysiol. 1996 Apr;101(2):105-9. PMID: 8647015; UI: 96245462.
A serial study of clinical and magnetic stimulation motor evoked potentials (MEP) was accomplished in 44 patients with the acute flaccid paralytic syndrome which occurred in Northern China in 1991. Control data were provided by 70 healthy subjects from the same area. The cases came from the same area where a so-called new “Chinese paralytic syndrome” had been reported. We found the clinical features of these 44 patients to be similar to those of classical Guillain-Barre. Prolongation of MEP latency at 2 sites or on 2 occasions was found in 36 patients of whom 26 showed obvious clinical and electrophysiological recovery within 4-8 weeks. Three cases showed reduced MEP amplitude with normal latency, but in 2 of them the amplitude recovered in 2-8 weeks. Only 2 cases had no response at all time. We think 41 patients (93.7%) had predominant nerve demyelination. The 3 other patients (6.8%) showed axonal degeneration which is within the range found in previous reports of classical Guillain-Barre. We conclude that the acute paralytic syndrome seen in the summer of 1991 in Northern China represents a classical Guillain-Barre syndrome with demyelination of motor and sensory fibers. There is no reason to consider any special nomenclature such as “Chinese paralytic syndrome” or “acute motor axonal neuropathy

Zhang X, et al. Guillain-Barre syndrome in six cities and provinces of northern China: is it a new entity? Chin Med J (Engl). 1995 Oct;108(10):734-8. Review. PMID: 8565657; UI: 96147668
Forty cases of Guillain-Barre Syndrome were reported, (GBS) which came from the regions where “Chinese Paralytic Syndrome” and “Acute Motor Axonal Neuropathy (AMAN)” were presented before. A study on their clinical, electrophysiological and pathological features was conducted, records on 3,733 GBS cases reported in northern China from 1978 to 1992 were reviewed and compared with cases of “acute moter axonal nouropathy”. The results showed that the clinical, electrophysiological and pathological features of GBS in north China are similar to those of typical GBS cases in western countries, though there seemed to be some special epidemiological features in age, seasonal and regional distribution. It was concluded that the GBS in northern China is demyelinating GBS dominantly, not a new entity.
Zhang Z, et al. [Risk factors for Guillain-Barre syndrome in northern China: a case-control study]. Chung Kuo I Hsueh Ko Hsueh Yuan Hsueh Pao. 1995 Aug;17(4):291-5. Chinese. PMID: 8575052; UI: 96147928.
We conducted a case-control study in northern China to estimate possible risk factors for Guillain-Barre Syndrome (GBS). Forty patients were consecutively seen at the PUMC hospital and the Second Hospital of Hebei Medical College between July and September 1991. The diagnosis was established following the NINCDS criteria for GBS. Among 36 patients with measurements of motor evoked potentials, 34 had evidences of demyelination. Eighty controls chosen from spouses or siblings, and neighbors or work/school mates, were matched by sex and age (+/- 3 years). Using the Mantel-Haenszel estimate of the odds ratio, cold rain, overloaded activities, a history of diarrhea, common cold, and exposure to organophosphorus one month before onset, significantly increased, at least six-fold, the risk for development of GBS. Cases and controls did not differ in the number of previous vaccinations. We suggest that a single antigent is less likely of etiological importance in GBS.
alth officials convinced the Chinese to rename the bulk of their polio to Guillaine Barre Syndrome (GBS). A study found that the new disorder (Chinese Paralytic syndrome) and the GBS was really polio (41). After mass vaccination in 1971, reports of polio went down but GBS increased about 10 fold.(Ref: Vaccination by Greg Beattie)