215

REVERSE TRENDELENBURG FOR NOCTURNALANGINA

SIR,-I read with interest the article by Dr Mohr and colleagues(June 12, p. 1325) on the value of tilting patients with nocturnalangina feet down at night. There is no doubt that haemodynamicchanges of heart failure occur during nocturnal angina, but is thiscause or effect? Seven of the ten patients studied had heart failure orleft-ventricular aneurysm to start with and further increases infilling pressure on lying down could have aggravated ischaemiainduced by some other mechanism. 1 It is also well known that manypainfree episodes of ischaemia occur at night.2 Such episodes couldbe modified by posture to the extent of becoming symptomatic.Mohr et al. have pointed out a useful therapeutic approach to

nocturnal angina, particularly in patients with poor ventricles.Caution should be exercised, however, before drawing anyconclusions from this work about the mechanisms behind thenocturnal angina.Department of Medicine,Northern General Hospital,Sheffield G. D. G. OAKLEY

SIR,-There is nothing new. For many years patients withcongestive heart failure and with angina were treated in a "cardiacchair". For reasons that have never been clear to me, this wonderfuldevice has disappeared from hospitals to be replaced by beds. Ratherthan treat angina with "reverse Trendelenburg tilt of the bed" asadvised by Dr Mohr and colleagues it could be as easy and wouldcertainly be as cheap to treat such patients in an old-fashionedarmchair.

Ambulatory Care Service,Albert Einstein College of Medicineof Yeshiva University,

Bronx Municipal Hospital Center,Bronx, N.Y. 10461, U.S.A. BERTRAND M. BELL

CEREBROSPINAL FLUID &ggr;-AMINOBUTYRIC ACIIVARIATIONS IN CEREBELLAR ATAXIA

SIR,-A major inhibitory neurotransmitter in mammals is

y-aminobutyric acid (GABA), and cerebrospinal fluid (CSF) GABAlevels may correlate with concentrations in brain tissue.3 DecreasedCSF GABA levels have been found in cerebellar degenerations.4,5However, we have found that the CSF GABA levels vary accordingto the type of spinocerebellar degeneration (table). Allmeasurements of CSF GABA levels were done by radioreceptorassay. 5The mean CSF GABA levels in patients with olivopontocere-

bellar atrophy (70 pmol/ml) and late cortical cerebellar atrophy (74pmollml) were significantly lower than normal (143 pmol/ml).However, in hereditary cerebellar ataxia (Sanger-Brown and Marie)patients, the mean CSF GABA level (139 pmol/ml) was normal.Olivopontocerebellar atrophy is characterised by cerebellar ataxia

and extrapyramidal symptoms and, histologically, by atrophiedganglion cells of the olives and grey-matter of the pons, followed bysecondary degeneration of Purkinje and other ganglion cells in thecerebellar cortex. These cellular changes suggest that the GABAconcentration in cerebellar tissue would be decreased. Moreover, inthis disease the pigmented cells of the substantia nigra, whichusually have high concentrations of GABA, show degenerativechanges so that the brain GABA concentration should be

1. Figueras J, Cinca J. Acute arterial hypertension during spontaneous angina in patientswith fixed coronary stenosis and exertional angina, an associated rather than atriggering phenomenon. Circulation 1981; 64: 60-80.

2. Oakley D, Al Janabi A. ST Segment depression in patients with severe angina pectoris.Br Heart J 1981; 45: 341.

3. Bohlen P, Hout S, Palfreyman MG. The relationship between GABA concentrationsm brain and cerebrospinal fluid. Brain Res 1979; 167: 297-305.

4. Manyam NVD, Katz L, Hare TA, Geber JC III, Grossman MH. Levels of&ggr;-aminobutyric acid in cerebrospinal fluid in various neurologic disorders. ArchNeurol 1980; 37: 352-55.

5. Kuroda H, Ogawa N, Yamawaki Y, Nukina I, Ofuji T, Yamamoto M, Otsuki S.Cerebrospinal fluid GABA levels in various neurological and psychiatric diseases. JNeurol Nerrosurg Psychiatry 1982; 45: 257-60.

CSF-GABA LEVELS IN NORMAL CONTROLS AND IN PATIENTS WITH

CEREBELLAR ATAXIAS

diminished. In late cortical cerebellar atrophy there is atrophy in thevermis and cerebellar hemispheres, with loss of Purkinje andgranular cells and secondary degeneration of the olivery nuclei. Inthis disease too GABA concentrations in cerebellar tissue should be

depressed. Thus, the diminished GABA levels in the brain mayaccount for the reduction in CSF levels in patients.In hereditary cerebellar ataxia, however, CSF GABA levels were

normal. The progression of this disease is slow and cerebellar

atrophy is less striking, there being severe spinal cord degeneration.Measurement of CSF GABA levels might help in the differential

diagnosis of cerebellar ataxias.

Institute for Neurobiology;Third Department of Internal Medicine;and Department of Neuropsychiatry,

Okayama University Medical School,2-5-1, Shikata-cho, Okayama 700, Japan

NORIO OGAWAHIROO KURODAZENSUKE OTAMITSUTOSHI YAMAMOTOSABURO OTSUKI

SHOSHIN BERIBERI

SIR,-Your June 5 editorial on cardiovascular beriberi did notmention two cases of shoshin beriberi described two years ago fromthis hospital. 1 These two fulminant cases of beriberi were studied indetail, with haemodynamic and plasma catecholamine data. Weknow of only two other published cases of shoshin beriberi withhaemodynamic studies-Jeffre3y and Abelman2 did a right heartcatheterisation and Attas et al., as your editorial notes, investigatedtheir case with right and left heart catheterisation and leftventricular angiography. Our haemodynamic data also showed anincrease in pulmonary wedge, pulmonary artery, and right atrialpressures. Systemic blood pressure was lowered despite a markedincrease in cardiac output, indicating decreased total peripheralresistance. The response ofhaemodynamic variables to intravenousthiamine was similar to that reported by Attas et al. After about 12 hsystemic blood pressure was normal but cardiac output remainedhigh. After 5-10 days of treatment cardiac output and total

peripheral resistance had returned to normal.We know of no other published data on catecholamine levels in

shoshin beriberi. In our two cases plasma catecholamines weregreatly increased (radioenzymatic determination). Despite this, totalperipheral resistance was low. This observation supports the view4that loss of control of muscle arteriolar tone is due to deficiency ofthiamine. 4 The cutaneous vasoconstriction that has beendemonstrated4 suggests that sympathomimetic amines in thissituation are active on the skin circulation.

Medical Resuscitation Service,Hôpital de Bicetre,94270 Le Kremlin Bicetre, France

C. RICHARDB. FONDPH. AUZEPY

1. Fond B, Richard C, Comoy E, Tillement JP, Auzepy P. Two cases of shoshin beriberiwith hemodynamic and plasma catecholamine data. Intens Care Med 1980; 6:193-98.

2. Jeffrey FE, Abelman WH. Recovery from proved shoalsin beriberi. Am J Med 1971; 50:123-28.

3. Attas M, Hanley HG, Stultz D. Fulminant beriberi heart diseaese with lactic acidosis,presentation of a case with evaluation of left ventricular function and review ofpathophysiologic mechanisms. Circulation 1978; 58: 566-72.

4. Blacket RB, Palmer AJ. Haemodynamic studies in high output beriberi. Br Heart J1960; 22: 483-501.