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aetiology of painful syndromes in diabetes mellitus. Itmay be that the reduction in pain tolerance is due torapid changes in blood glucose rather than persistenthyperglycaemia. The findings of Morley et all’ supportthis notion since maximum tolerated pain did notreturn to normal until at least thirty minutes after theglucose infusion, during which time blood glucoseconcentrations would still have been falling. Rapidfluxes in blood glucose might explain the onset ofpainful neuropathic symptoms after institution of

therapy, as reported earlier ,18Painful diabetic neuropathies are of multifactorial

aetiology, but there is much evidence that chronic

hyperglycaemia with its metabolic consequences is themost important ingredient.2 Further work is needed onthe association between hyperglycaemia, painperception, and possible glucose modulation of opioidreceptors. Investigations on the possible influence ofblood glucose flux on the spontaneous activity inprimary nociceptive afferent fibres in experimentalneuropathy would be of particular interest, as an

alternative mechanism whereby changes in blood

glucose levels might influence pain. Blood glucose fluxcould conceivably lead to alteration in the level of nervefibre potassium or other ions, and these changes mightalter resting membrane potential. The findings ofMorley et all ’ also have implications for clinical trialsof other agents in the treatment of symptomaticneuropathy. Before claiming therapeutic benefit,investigators will have to show that there are no

changes in glycaemic control during the drug trial.Two studies on the effects of aldose reductaseinhibitors in painful diabetic neuropathy have

produced conflicting results about symptomaticrelief, 11,20 and a possible explanation for such

discrepancies is a difference in the degree of glycaemiccontrol. We need more information on the relationbetween fluctuations in blood glucose and paintolerance in diabetic subjects. Whether or not thesenew observations are relevant to the routine

management of painful neuropathy, any diabetic

patient with symptomatic neuropathy should beoffered the best blood glucose control that isachievable.

Respiratory Function in ScoliosisWHY do some individuals with scoliosis progress to

respiratory failure and cor pulmonale when others,apparently similar, do not? Does the fault lie in amechanical abnormality of the chest wall itself, inweakness or fatigue of respiratory muscles, in

18 Ellenberg M. Diabetic neuropathy precipitating after institution of diabetic control.Am J Med Sci 1958; 236: 466-71

19. Young RJ, Ewing DJ, Clarke BF. A controlled trial of sorbinil, an aldose reductaseinhibitor, in chronic painful diabetic neuropathy. Diabetes 1983; 32: 938-42.

20 Lewin IG, O’Brien IAD, Morgan MH, Corrall RJM. Clinical and electrophysiologicalstudies with the aldose reductase inhibitor, sorbinil, in symptomatic diabeticneuropathy Diabetologia 1984; 26: 445-48.

histological or developmental abnormalities of thelungs themselves, or in a defective respiratory drive?The structural abnormalities are the most obviousculprit, particularly in patients with high thoraciccurves. The lateral rotation of the spine causes the ribsto protrude posteriorly forming a hump, and the angleof articulation of the ribs and spine is grossly distorted.The severity of the lateral curvature is easily measuredby the Cobb angle; but the rotation, which is probablymore important, is not and inability to measure it hasbeen an obstacle to comparisons between patients.Some progress, however, has been made. Cooper

et all. studied 29 patients with thoracic adolescentidiopathic scoliosis of less than 60° and found thatmaximum inspiratory pressure (I max) was decreasedbut maximum expiratory pressure (Pe max) was normal.They argue that, if the expiratory muscles are normal,the inspiratory muscles are probably normal as welland their explanation for the low PI max is that the

inspiratory muscles work at a mechanical disadvantagebecause of the chest deformity. These assumptionsmay well be only partly valid but there is no doubt thatthe severity of the scoliosis itself is also closely relatedto other lung function abnormalities such as thedecrease in total lung capacity (TLC), functionalresidual capacity (FRC), residual volume (RV), andvital capacity (VC).About 80% of scolioses are idiopathic, but this leaves

a substantial number in which the spinal curvature iseither due to or accompanies weakness of the

respiratory muscles, often as part of a generalised orproximal myopathy although in some areas of theworld poliomyelitis is still a common cause. These

’patients have a lower TLC, FRC, and VC for a givenangle of scoliosis than non-paralytic scoliotics and theirPl max

and Pe max are also lower than normal. For

unknown reasons the compliance of the chest wall inpatients with respiratory muscle weakness is alsodiminished.2 The outlook for the patient is much

poorer if muscle weakness is present than if it is not.Clinicians must be especially alert to the possibility ofdiaphragm weakness, which may be signalled by severeorthopnoea and is confirmed by a drop of around 50%in VC when the patient lies flat. The contribution ofmuscle fatigue to respiratory dysfunction is less

certain, and there is no way of measuring it routinely.Fatigue does seem likely to be important in respiratoryfailure, particularly in acute-on-chronic respiratoryfailure precipitated, for instance, by chest infections.The shape of the thoracic cage in scoliosis is

determined largely by the musculo-skeletal mechanics,and the lungs adapt to the bony configurationthroughout growth. This leads to gross distortion insevere cases but we still do not know the importance of

1. Cooper DM, Rojas JV, Mellins RB, Keim HA, Mansell AL. Respiratory mechanics inadolescents with idiopathic scoliosis Am Rev Resp Dis 1984; 130: 16-22.

2. Estenne M, Heilporn A, Delhez L, Yernault JC, de Troyer A. Chest wall stiffness inpatients with chronic respiratory muscle weakness. Am Rev Resp Dis 1983; 128:1002-07

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developmental abnormalities in progression to

respiratory and cardiac failure. In congenital scoliosisof early onset there seems to be failure of alveolarmultiplication,3 whereas in idiopathic scoliosis thealveoli do not enlarge normally.4 4 Histologicalexamination, however, will often reveal remarkablylittle abnormality. There is a wider than usual variationin alveolar size but the pulmonary microcirculationdevelops in parallel with the alveoli. This importantfinding is backed by isotope studies showinghomogeneous ventilation and perfusion. Nevertheless,scoliotics often have a low pO in the presence of anormal pC02, presumably indicating ventilation/

perfusion mismatch.For many years emphysema was believed to be a

feature of the scoliotic chest, but in fact there is seldomevidence of airways disease. Nonetheless, lungcompliance is commonly subnormal, possibly becauseof small-airways collapse due to inability to take a deepbreath or sigh. This defect is most pronounced inscoliotics with muscle weakness. Lung compliance canbe increased by positive-pressure ventilation.5One attractive proposition is that respiratory failure

develops because of defective respiratory drive; andcertainly the respiratory drive, as measured byrebreathing CO techniques, is often subnormal. 6

Interpretation is difficult, however, because the

rebreathing test measures both the respiratory centre’soutput and the ability of the chest wall muscles to effectventilation. In other words, it reflects both themechanical properties of the thorax and the function ofthe respiratory centre. The degree of abnormality inventilatory response is proportional to VC and to thecompliance of the chest wall and lungs. Thus, unlessrespiratory centre failure is proportional to the chestwall abnormality the major determinants of the CO2response are the mechanical properties of the thorax.We still do not know whether the respiratory centrefunctions normally or not in idiopathic scoliosis.

Furthermore, many central-nervous-system diseasescausing scoliosis, such as poliomyelitis, may inthemselves be associated with diminished respiratorydrive.

It has become increasingly apparent that respiratoryfailure in scoliosis initially occurs at night,’ and

especially during rapid-eye-movement sleep. Thefactors here probably include a diminished O2 andCO 2 sensitivity during sleep, ventilation/

perfusion mismatch, and upper airways obstruction.Nocturnal hypoxaemia seems very important in thedevelopment of right heart failure, with hypoxic

3. Boffa P, Stovin P, Shneerson J Lung developmental abnormalities in severe scoliosis.Thorax 1984, 39: 681-82

4 Olgiati R, Levine D, Smith JP, Briscoe WA, King TKC. Diffusing capacity inidiopathic scoliosis and its interpretation regarding alveolar development. Am RevResp Dis 1982; 126: 229-30.

5 Sinha R, Bergofsky EH. Prolonged alteration of lung mechanics in kyphoscoliosis bypositive pressure hyperinflation. Am Rev Resp Dis 1972, 106: 47-57

6 Kafer ER. Idiopathic scoliosis. Mechanical properties of the respiratory system and theventilatory response to carbon dioxide. J Clin Invest 1975; 55: 1153-63

7 Guilleminault C, Kurland G, Winkle R, Miles LE. Severe kyphoscoliosis, breathing,and sleep "Quasimodo" syndrome during sleep. Chest 1981; 79: 626-30

vasoconstriction causing pulmonary hypertension.Patients commonly die at night from hypoxic cardiacarrhythmias. Daytime hypoxaemia also leads to

pulmonary hypertension and later cor pulmonale, butthe rate of rise in pulmonary artery pressure during andafter exercise is more closely related to the lung volumeas measured by VC, FRC, or TLC .8 The rate of rise ofpulmonary artery pressure during exercise is

particularly steep if the vital capacity is less than 1’ 5litres. Thus, some restrictions on exercise are

justifiable, particularly if the pO 2 is also low. Theexercise ability of severe scoliotics is also unusual inthat it is limited by ventilatory factors-whereas innormal subjects it is limited by the circulation.Maximum exercise ventilation, like the rate of rise ofpulmonary artery pressure, correlates well with thevital capacity.9Lung size, therefore, determines many aspects of

respiratory function and pulmonary hypertension inscoliosis. But lung size is itself dependent on the shapeof the thorax and ultimately on the mechanical forcesthat initially caused the spinal curvature. Mechanicalfactors are the primary abnormality to which so manyof the physiological abnormalities relate, and it is

disappointing that quantification, particularly of therotation of the spine, is still so difficult. Prediction ofwhich patients will proceed to respiratory or cardiacfailure is still imprecise, but for the clinician the bestindices are the level and severity of the scoliosis (asmeasured by the Cobb angle), VC, the resting arterialpO 2 during the day and at night, and the presence orabsence of muscular weakness.

Uncomfortable ImagesPEOPLE spend more time gazing at the screens of

television receivers and visual display units now thanever before, because it is their work or their

amusement-or, for a few fortunate souls, both

together. As work, it can be very exacting. The screen,regarded as a printed page, is still a typographer’snightmare, even after decades of technical

improvement. What it shows, none too legibly, may becryptic or frustrating in varying degree. Patience andtolerance may be overtaxed. They may equally beovertaxed by many other stresses in commercial life.But are there more specific hazards? The most

completely authenticated is photosensitive epilepsy. Inabout 3% of epileptics,’ the seizures are induced

especially by flickering such as is produced by thescreen display; and the image can readily be varied toshow what characteristics of the display are most liableto induce a seizure. In general, flicker at 15-20 per

8. Shneerson JM Pulmonary artery pressure in thoracic scoliosis during and after

exercise while breathing air and pure oxygen Thorax 1978; 33: 747-549 Shneerson JM. The cardiorespiratory response to exercise in thoracic scoliosis Thorax

1978, 33: 457—63.1. Jeavons PM, Harding GFA Photosensitive epilepsy London: Heinemann, 1975