CEREBROSPINAL FLUID γ-AMINOBUTYRIC ACII VARIATIONS IN CEREBELLAR ATAXIA
1
215 REVERSE TRENDELENBURG FOR NOCTURNAL ANGINA SIR,-I read with interest the article by Dr Mohr and colleagues (June 12, p. 1325) on the value of tilting patients with nocturnal angina feet down at night. There is no doubt that haemodynamic changes of heart failure occur during nocturnal angina, but is this cause or effect? Seven of the ten patients studied had heart failure or left-ventricular aneurysm to start with and further increases in filling pressure on lying down could have aggravated ischaemia induced by some other mechanism. 1 It is also well known that many painfree episodes of ischaemia occur at night.2 Such episodes could be 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 any conclusions from this work about the mechanisms behind the nocturnal angina. Department of Medicine, Northern General Hospital, Sheffield G. D. G. OAKLEY SIR,-There is nothing new. For many years patients with congestive heart failure and with angina were treated in a "cardiac chair". For reasons that have never been clear to me, this wonderful device has disappeared from hospitals to be replaced by beds. Rather than treat angina with "reverse Trendelenburg tilt of the bed" as advised by Dr Mohr and colleagues it could be as easy and would certainly be as cheap to treat such patients in an old-fashioned armchair. Ambulatory Care Service, Albert Einstein College of Medicine of Yeshiva University, Bronx Municipal Hospital Center, Bronx, N.Y. 10461, U.S.A. BERTRAND M. BELL CEREBROSPINAL FLUID &ggr;-AMINOBUTYRIC ACII VARIATIONS IN CEREBELLAR ATAXIA SIR,-A major inhibitory neurotransmitter in mammals is y-aminobutyric acid (GABA), and cerebrospinal fluid (CSF) GABA levels may correlate with concentrations in brain tissue.3 Decreased CSF GABA levels have been found in cerebellar degenerations.4,5 However, we have found that the CSF GABA levels vary according to the type of spinocerebellar degeneration (table). All measurements of CSF GABA levels were done by radioreceptor assay. 5 The mean CSF GABA levels in patients with olivopontocere- bellar atrophy (70 pmol/ml) and late cortical cerebellar atrophy (74 pmollml) 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 atrophied ganglion cells of the olives and grey-matter of the pons, followed by secondary degeneration of Purkinje and other ganglion cells in the cerebellar cortex. These cellular changes suggest that the GABA concentration in cerebellar tissue would be decreased. Moreover, in this disease the pigmented cells of the substantia nigra, which usually have high concentrations of GABA, show degenerative changes so that the brain GABA concentration should be 1. Figueras J, Cinca J. Acute arterial hypertension during spontaneous angina in patients with fixed coronary stenosis and exertional angina, an associated rather than a triggering 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 concentrations m 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. Arch Neurol 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. J Neurol 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 the vermis and cerebellar hemispheres, with loss of Purkinje and granular cells and secondary degeneration of the olivery nuclei. In this disease too GABA concentrations in cerebellar tissue should be depressed. Thus, the diminished GABA levels in the brain may account 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 OGAWA HIROO KURODA ZENSUKE OTA MITSUTOSHI YAMAMOTO SABURO OTSUKI SHOSHIN BERIBERI SIR,-Your June 5 editorial on cardiovascular beriberi did not mention two cases of shoshin beriberi described two years ago from this hospital. 1 These two fulminant cases of beriberi were studied in detail, with haemodynamic and plasma catecholamine data. We know of only two other published cases of shoshin beriberi with haemodynamic studies-Jeffre3y and Abelman2 did a right heart catheterisation and Attas et al., as your editorial notes, investigated their case with right and left heart catheterisation and left ventricular angiography. Our haemodynamic data also showed an increase in pulmonary wedge, pulmonary artery, and right atrial pressures. Systemic blood pressure was lowered despite a marked increase in cardiac output, indicating decreased total peripheral resistance. The response ofhaemodynamic variables to intravenous thiamine was similar to that reported by Attas et al. After about 12 h systemic blood pressure was normal but cardiac output remained high. 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 were greatly increased (radioenzymatic determination). Despite this, total peripheral resistance was low. This observation supports the view4 that loss of control of muscle arteriolar tone is due to deficiency of thiamine. 4 The cutaneous vasoconstriction that has been demonstrated4 suggests that sympathomimetic amines in this situation are active on the skin circulation. Medical Resuscitation Service, Hôpital de Bicetre, 94270 Le Kremlin Bicetre, France C. RICHARD B. FOND PH. AUZEPY 1. Fond B, Richard C, Comoy E, Tillement JP, Auzepy P. Two cases of shoshin beriberi with 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 of pathophysiologic mechanisms. Circulation 1978; 58: 566-72. 4. Blacket RB, Palmer AJ. Haemodynamic studies in high output beriberi. Br Heart J 1960; 22: 483-501.
Transcript of CEREBROSPINAL FLUID γ-AMINOBUTYRIC ACII VARIATIONS IN CEREBELLAR ATAXIA
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.
![Significance of β-actin gene in Cerebrospinal fluid …...Sharma et al./Vol. VIII [1] 2017/168 – 178 169 Mycobacterium tuberculosis from cerebrospinal fluid, pathologic biochemical](https://static.fdocument.org/doc/165x107/5fce2ad2daf862618f056227/significance-of-actin-gene-in-cerebrospinal-fluid-sharma-et-alvol-viii.jpg)
