Abstract
We examined four patients with fluorosis, presenting with compressive myelopathy, by MRI, using spin-echo and fast low-angle shot sequences. Cord compression due to ossification of the posterior longitudinal ligament (PLL) and ligamentum flavum (LF) was demonstrated in one and ossification of only the LF in one. Marrow signal was observed in the PLL and LF in all the patients on all pulse sequences. In patients with compressive myelopathy secondary to ossification of PLL and/or LF, fluorosis should be considered as a possible cause, especially in endemic regions.
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Ossification of the posterior longitudinal ligament and fluorosis
There is only one report of ossification of the posterior longitudinal ligament (OPLL) in patients suffering from fluorosis. Deshpande, Dinakarand Reddy (1976) mention an association with fluorosis in 14 of 26 cases. OPLL is not mentioned in two reviews of fluorosis (Jolly 1981; Reddy and Reddy 1987). Patients. In our neurological service,
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Posttraumatic pseudomenigocoele of cervical spine in a patient with skeletal fluorosis. Case report
A case of fluorotic cervical compressive myelopathy precipitated by trauma is reported. The delayed neurological deterioration was due to a posttraumatic pseudomenincocele, the prompt treatment of which resulted in recovery. Posttraumatic pseudomeningocele is very rate; and certainly so in fluorosis, and thus has not been reported in the literature to date.
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Fluorotic cervical compressive myelopathy, 20 years after laminectomy: A rare event
BACKGROUND: Spinal cord compression in flourosis is a common complication. These complications are mainly due to compression of the spinal cord by thickening and ossification of posterior longitudinal ligament and ligamentum flavum. Surgical decompression is the treatment of choice for fluorotic spinal cord compression. The recurrence of spinal cord compression
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Endemic fluorosis presenting as cervical cord compression
Neurological involvement in fluorosis occurs in the advanced stage of the disease and is due to compression of the spinal cord and/or nerve roots. There are only a few reports on the role of surgical management of these cases in the medical literature. Five cases of fluorosis from the endemic areas of Uttar Pradesh,
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Fluorosis in Nalgonda District, Hyderabad-Deccan
Details of inviestigations of 32 cases of skeletal fluorosis with neurological manifestations are described. The results of the eighth-nerve functions are reported. The probable factors responsible for early skeletal changes in patients from Kamaguda are discussed. A case is described in which excretion of previously stored fluoride continued in the
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Fluoride & Osteoarthritis
While the osteoarthritic effects that occurred from fluoride exposure were once considered to be limited to those with skeletal fluorosis, recent research shows that fluoride can cause osteoarthritis in the absence of traditionally defined fluorosis. Conventional methods used for detecting skeletal fluorosis, therefore, will fail to detect the full range of people suffering from fluoride-induced osteoarthritis.
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Skeletal Fluorosis: The Misdiagnosis Problem
It is a virtual certainty that there are individuals in the general population unknowingly suffering from some form of skeletal fluorosis as a result of a doctor's failure to consider fluoride as a cause of their symptoms. Proof that this is the case can be found in the following case reports of skeletal fluorosis written by doctors in the U.S. and other western countries. As can be seen, a consistent feature of these reports is that fluorosis patients--even those with crippling skeletal fluorosis--are misdiagnosed for years by multiple teams of doctors who routinely fail to consider fluoride as a possible cause of their disease.
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"Pre-Skeletal" Fluorosis
As demonstrated by the studies below, skeletal fluorosis may produce adverse symptoms, including arthritic pains, clinical osteoarthritis, gastrointestinal disturbances, and bone fragility, before the classic bone change of fluorosis (i.e., osteosclerosis in the spine and pelvis) is detectable by x-ray. Relying on x-rays, therefore, to diagnosis skeletal fluorosis will invariably fail to protect those individuals who are suffering from the pre-skeletal phase of the disease. Moreover, some individuals with clinical skeletal fluorosis will not develop an increase in bone density, let alone osteosclerosis, of the spine. Thus, relying on unusual increases in spinal bone density will under-detect the rate of skeletal fluoride poisoning in a population.
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Fluoride & Spinal Stenosis
Spinal stenosis is a narrowing of the spaces in the spine that results in pressure being placed on the spinal cord and/or nerve roots. Although stenosis can develop without symptoms, it may produce numbness, tingling, pain and difficulty in walking, as well as a heavy/tired feeling in the legs. It is estimated that 250,000 to 500,000 Americans currently have symptoms of spinal stenosis. Skeletal fluorosis is one cause of stenosis.
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X-Ray Diagnosis of Skeletal Fluorosis
In 1937, Kaj Roholm published his seminal study Fluorine Intoxication in which he described three phases of bone changes that occur in skeletal fluorosis. (See below). These three phases, which are detectable by x-ray, have been widely used as a diagnostic guide for detecting the disease. They describe an osteosclerotic bone disease that develops first in the axial skeleton (the spine, pelvis, and ribs), and ultimately results in extensive calcification of ligaments and cartilage, as well as bony outgrowths such as osteophytes and exostoses. Subsequent research has found, however, that x-rays provide a very crude measure for diagnosing fluorosis since the disease can cause symptoms and effects (e.g., osteoarthritis) before, and in the absence of, radiologicaly detectable osteosclerosis in the spine.
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