The treatment of acute low back pain--bed rest, exercises, or ordinary activity?

BACKGROUND: Bed rest and back-extension exercises are often prescribed for patients with acute low back pain, but the effectiveness of these two competing treatments remains controversial. METHODS: We conducted a controlled trial among employees of the city of Helsinki, Finland, who presented to an occupational health care center with acute, nonspecific low back pain. The patients were randomly assigned to one of three treatments: bed rest for two days (67 patients), back-mobilizing exercises (52 patients), or the continuation of ordinary activities as tolerated (the control group; 67 patients). Outcomes and costs were assessed after 3 and 12 weeks. RESULTS: After 3 and 12 weeks, the patients in the control group had better recovery than those prescribed either bed rest or exercises. There were statistically significant differences favoring the control group in the duration of pain, pain intensity, lumbar flexion, ability to work as measured subjectively, the Oswestry back-disability index, and number of days absent from work. Recovery was slowest among the patients assigned to bed rest. The overall costs of care did not differ significantly among the three groups. CONCLUSIONS: Among patients with acute low back pain, continuing ordinary activities within the limits permitted by the pain leads to more rapid recovery than either bed rest or back-mobilizing exercises.

Sorbitol and myoinositol levels in the cerebrospinal fluid of diabetic patients.

Sorbitol and myoinositol have been measured from human cerebrospinal fluid. The normal concentrations are very small (below 100 microM/l). The detection limit of the Gas Liquid Chromatographic method was 5 microM/l. The sensitive method provided a possibility to compare quantitatively the sugar alcohol concentrations in human cerebrospinal fluid. Sorbitol concentration was increased and myoinositol concentration decreased in the cerebrospinal fluid of diabetic patients.

Myoinositol and function of peripheral nerves in human diabetics. A controlled clinical trial.

Fifty-nine diabetic patients participated in a double-blind study in order to evaluate the efficiency of myoinositol to improve the function of peripheral nerves. Myoinositol in the amounts given was not able to change motor conduction velocity or vibratory perception threshold. No change in retinopathy and several biochemical parameters was observed.

Gas chromatographic separation and mass spectrometric identification of polyols in human cerebrospinal fluid and plasma.

Seven polyols, erythritol, arabinitol, anhydroflucitol, mannitol, sorbitol, myoinositol and possibly ribitol were identified in human cerebrospinal fluid by means of gas-liquid chromatography and mass spectrometry. Quantitative data were obtained for five polyols, arabinitol, anhydroglucitol, mannitol, sorbitol and myoinositol, by screening of 205 CSF samples. These five polyols represented 90-95 per cent of the polyol-concentration which was 340 +/- 105 mumol/1 in the total series. The concentration of polyols in the CSF was two times higher than that in the plasma (148 +/- 30 mumol/1), where only anhydroglucitol and myoinositol could be quantitated. The variations noted were not associated with age, sex or the plasma concentrations of polyols. The polyols of the CSF most likely originate from brain tissue and/or spinal cord since penetration from the plasma against a gradient seems unlikely.

Polyols in the cerebrospinal fluid and plasma of neurological, diabetic and uraemic patients.

Five polyols, arabinitol, anhydroglucitol, mannitol, sorbitol and myoinositol, normally present in the cerebrospinal fluid (CSF), were studied. Quantitative gas-liquid chromatographic analysis of 211 CSF and 112 plasma samples indicated significantly altered concentrations in several clinical conditions. All five polyols were decreased in the CSF of patients suffering from meningitis, cerebral atrophy, sepsis, and in patients receiving intrathecal cytostate therapy. Equilibration between plasma and CSF may explain the changes in sepsis and meningitis, while decreased total number of functioning cells may cause the decrease in cerebral atrophy. Intrathecal cytostates seem to have a destroying effect on the cell metabolism of the central nervous system. Renal failure causes accumulation of polyols in the plasma. Alterations in the metabolism of sorbitol, myoinositol and anhydroglucitol seem to be present in diabetes. The plasma concentration of anhydroglucitol is decreased in renal failure.

Accumulation of myoinositol in plasma and red cells of diabetic patients.

The concentration of myoinositol in plasma, cerebrospinal fluid and red cells and its elimination by the kidneys have been studied in 51 diabetic patients with normal or impaired kidney function, 16 non-diabetic patients with renal failure and 37 healthy controls. All diabetic patients who had a glomerular filtration rate considerably below normal, was the plasma concentration of myoinositol higher than in controls. The findings show that the rise in plasma concentration of myoinositol most probably results from a decreased glomerular filtration rate. In diabetic patients, urinary excretion of myoinositol correlated with an exponential increase in glucose excretion. That myoinositol accumulates in red cells of diabetic patients may be the result of its retention within these cells caused primarily by a transient, abnormal increase in the plasma concentration of myoinositol after an average meal.

Cerebrospinal fluid sorbitol and myoinositol in diabetic polyneuropathy.

Changes in cerebrospinal fluid (CSF) concentrations of sorbitol and myoinositol in 21 patients with diabetic polyneuropathy were studied with gas-liquid chromatography. The sorbitol concentration was significantly increased in diabetic patients with elevated plasma glucose. Myoinositol concentration was significantly decreased in patients with polyneuropathy compared with the controls. Both alterations in polyol concentrations of the CSF were present already two months from onset of symptoms of diabetes. Patients with peripheral polyneuropathy receiving oral hypoglycemic drugs did not have elevated plasma glucose and CSF sorbitol levels, but showed significantly decreased CSF myoinositol concentrations compared with the controls. These observations suggest that myoinositol concentration may be decreased in the central nervous system in adult onset mild diabetes with normal plasma glucose and that the decrease in the myoinositol in CSF possibly is connected with the development of neuropathy.

Plasma, red cell and cerebrospinal fluid concentrations of mannitol and sorbital in patients with severe chronic renal failure.

The concentrations of mannitol and sorbitol in plasma, red cells, cerebrospinal fluid and urine were determined in 24 patients with chronic renal failure; 10 of them were on conservative treatment and 14 were haemodialysed three times weekly. The mannitol concentration was significantly increased in the plasma and the cerebrospinal fluid of the uraemic patients compared with the controls. In six out of ten uraemic patients mannitol clearance values exceeded creatinine clearance values. The plasma concentration of sorbitol was undetectable or very low in all patients and control subjects. Red-cell and cerebrospinal fluid concentrations of sorbitol showed a large individual variation in the uraemic patients on conservative treatment and did not correlate with kidney function. During dialysis the mannitol concentration decreased, leading to a small osmotic gradient between the plasma and the red cells. The changes in the concentration of mannitol during dialysis showed no connection with the symptoms of central nervous disturbance which appeared during dialysis treatment. The red cell sorbitol concentration during dialysis increased by about 20%. There was a correlation (p less than 0.05) between t,e increase in sorbital in cereemic patients.

Plasma, red cell and cerebrospinal fluid concentrations of myoinositol in patients with severe chronic renal failure.

A study was made of 24 patients with severe chronic renal failure; 14 of them were undergoing regular haemodialysis treatment 3 times weekly. Plasma, red-cell and cerebrospinal fluid concentrations of myoinositol were increased in all the patients treated conservatively. The plasma level of myoinositol correlated with the plasma level of creatinine (r = 0.78). The plasma myoinositol level increased more than the CSF and red-cell levels, indicating that the myoinositol in the red cells and the CSF originated mostly in plasma. Dialysis for eight hours produced a fall of about 50% in the level of myoinositol in plasma while the decrease in red-cell myoinositol was negligible. This lead to an osmotic grandient between extra- and intra-cellular myoinositol which was however small in molar terms and did not correlate with symptoms of central neurological disturbances.

Variation in polyol levels in cerebrospinal fluid and serum in diabetic patients.

Cerebrospinal fluid (CSF) or CSF and plasma levels of sorbitol, 1,5-anhydroglucitol and myoinositol of diabetic and non-diabetic patients with normal kidney function and of diabetic and non-diabetic patients with impaired kidney function were measured by gas-liquid chromatography. The CSF sorbitol level correlated with the plasma glucose level (p less than or equal to 0.05) in diabetic patients with normal kidney function, having received insulin for less than 12 months. The correlation between CSF sorbitol and plasma glucose levels in patients not dependent on insulin was not significant. Sorbitol was not detected in the plasma. The highest sorbitol levels in CSF were seen in insulin-dependent diabetic patients with impaired kidney function. No rise was seen in non-diabetic uremia. 1,5-anhydroglucitol, normally present in plasma, was absent from CSF and plasma in diabetic patients receiving insulin. In non-diabetic uremic patients, 1,5-anhydroglucitol levels in CSF and plasma were lower than in healthy subjects, but htere was no correlation with plasma glucose levels. The myoinositol level was higher in CSF than in the plasma of both non-diabetic and diabetic patients with normal kidney function. Both plasma and CSF levels were significantly (p less than 0.001) elevated in diabetic as well as in non-diabetic uremic patients, the plasma myoinositol increasing relatively more than the CSF levels. The elevation of plasma myoinositol correlated with the elevation of plasma creatinine and thus also with the impairment of kidney function. Plasma and CSF myoinositol levels were not influenced by the plasma glucose level.