BIOL PSYCHIATRY 1992;31:735-738
"735
BRIEF REPORTS
Subcorticai Brain Anatomy in Anorexia and Bulimia Mustafa M. Husain, Kevin J. Black, P. Murali Doraiswamy, Sunjay A. Shah, W. J. Kenneth Rockwell, Everett H. Ellinwood, Jr., and K. Ranga Rama Krishnan
Introduction Many studies have reported a generalized decrease in brain volume ("pseudoatrophy") in patients with anorexia nervosa and bulimia (Enzmann and Lane 1977; Heinz et al 1977; Hoffman et al 1989a and b; Krieg et al 1989b). To some degree this change is reversible, but some enlargement of cerebrospinal fluid (CSF) spaces appears to persist despite normalization of weight and eating habits (Artmann et al 1985; Krieg et al 1986, 1988). Change that persists after successful treatment might be due to residual damage to the brain or persistent abnormal metabolism; however, it might also represent underdeveloped or involuted areas that were originally responsible for the behavioral pathology (Artmann et al 1985). However, previous in vivo anatomic studies have focused only on the gross finding of CSF space enlargement or have used techniques with poor spatial resolution and partial voluming problems (i.e., single photon emission computed tomography (SPECT); Krieg et al 1989a). Limited studies of regional cerebral metabolism have shown focal changes: one small positron From the Department of Psychiatry, Duke University Medical Center, Durham. NC (MMH, PMD. WJKR, EHE, KRRK), Washington University School of Medicine. St. Louis, MO (KIB). School of Medicine, U "ive~;ty of North Carolina. Chapel Hill, NC (SAS), and University of Texas Southwestern Medical School, Dallas, TX (MMH). Address reprint requests to Dr. Everett H. Ellinwood. Department of Psychiatry, Box 3870, Duke University MeJical Center, Durham, NC 27710. Received May 20, 1991; revised November I, 1991.
© 1992 Society of Biological Psychiatry
emission tomography (PET) study of anorexia (Herholz et ai 1987) suggested focal metabolic abnormalities in the striatum, tempotal cortex, thalamus, and brainstem; and a study comparing magnetic resonance imaging (MRI) Tt values in bulimics and controls found a significant difference in the inferior frontal lobe, but not in other brain regions surveyed (Hoffman et al 1990). Because Herholz et al have reported focal metabolic abnormalities in the basal ganglia we decided to assess changes in midline subcortical structures and brainstem in patients with eating disorder.
Methods
Subjects Patients were 24 women undergoing treatment at the Duke University Medical Center Eating Disorders Unit, who had received diagnoses of anorexia nervosa (n = 12) or bulimia (n = 12) by DSM-III criteria. Average age was 25.3 .47 years (SD) for anorectics and 24.5 __ 4 years for bulimics. One of the anorectic patients had a bingeing episode. None of the bulimics had a past history of anorexia nervosa. Four of the 12 bulimic and 11 of the 12 anorectic patients had menstrual dysfunction. The average duration of the illness in bulimics was 88.7 __ 45 months. The average duration of the illness in anorectics was 62.7 _ 52.36 months. Controls were 11 normal subjects screened 0006-3223/92/$05.00
736
Brief Reports
BIOLPSYCHIATRY 1992;31:735-738
for psychiatric disorders. Average age for controis was 27.8 ___ 6 years. Clinical characteristics of these subjects have been described previously (Doraiswamy et al 1990, 1991). The weight (lbs)/height (kiches) ratio for anorectics (1.41 -_. 0.24) was smaller than for controls (1.88 ± 0.14)and bulimics (2.04 --+ 0.36) (F = 13.59, df = 2, p < 0.0001). Post hoe testing confirmed this finding.
Image Acquisition MRI was performed on a 1.5 Tesla General Electric (Milwaukee, Wl). Scans were performed with the subject's head positioned with the canthomeatal line at zero degrees from the vertical axis and the imager's grid centered at the nasion. Midsagittal T~ weighted images were selected as previously described (Doraiswamy et al 1990). Scans that did not result in a midline image (failed to demonstrate the cerebral aqueduct) or did not contain the entire intracranial area in the scanning window were not included in the study.
Image Analysis The following cross-sectional area and distance measurements were performed on each midsagittal scan: corpus callosum (length, width, and area); cerebral cortex (,area); septum peilucidum (area); thalamus (area); fourth ventricle (area); midbrain and pens (areas). The areas were defined using a standard MRi atlas (Brant-Zawadski Man, t Norman D 1987). Regions of interest were traced and measured using standard Signa offline software (Doraiswamy et al 1990). Midbrain asse~Isment was made using a standard MRI atlas (Brant-Zawadski M and Norman D 1987). The upper extent of the colliculi was used to determine the upper border and the bulge of the pens t~determine the lower border of the midbrain. All tracings were conducted blind to the diagnosis. Corpas callosum (CC) measurements were chosen relative to the longest (A-P) axis, starting from the most anterior and most posterior reaches of the internal (inferior)border
of the CC. The "middle" thickness was measured perpendicular to the longest axis at a point halfway between the anterior and posterior poles of the CC.
Statistical Methods Data were analyzed using PC-SAS (SAS Institute, Cary, NC). Group comparisons were made with analysis of variance (ANOVA) and post hoe tests; and correlation between variables was assessed with Pearson's Correlation Coefficient. Normality of distribution was assessed using Shapiro Wilk statistic and when the assumption was not satisfied, nonparamelric tests were used.
Results There was no significant difference in age of subjects by diagnosis. Table l summarizes the measurements of different midsagittal brain structures in all three groups. The most significant finding in this study was the smaller thalamus area in anorectic (1.4 __ 0.5 cm2) patients as compared with bulimics (1.9 -+ I cm 2) and controls (I.93 ± 0.4 cm 2) (F -- 4.88, p = 0.01). These differences were confirmed by post hoc tests. The midbrain area was also significantly smaller in anorectic (2.17 -+ 0.35 cm 2) patients as compared with bulimics (2.48 __ 0.23 cm2) and controls (2.54 ± 0.35 cm2) (F - 4.47, p - 0.01)(see Table 2). Bulimics did not differ from controls. The anorectic who also had bingeing did not differ from the other anorectic patients. There was no correlation between body weight, duration of illness, thalamus, and midbrain. The ratio of the thalamus/cerebral hemisphere, were significantly different between patients and controls ( F = 4.06, df -- 2, p < 0.04). The significance was due to differences between anorectics and controls. The ratio of the midbrain/cerebral hemisphere was also different between p,ttients and controls (F = 19.3, df -- 2, p < 0.0001). The differences were confirmed by post hoc tests to be due to the anorectic subjects.
Brief Reports
n10LPSYCHIATRY
737
1992 ;31:735 -738
Table !. MRI Measurements in Anorectics, Bulimics, and Controls
Age (yr) Weight (Ibs) C.C. area (era 2) C,C. length (cm) C.C. widlh (cm) Sep Pel (cm") Thalamus (cm') Midbruin (cm') Ports (cm2) IVth vent (cm~)
Thalamus/cerebrum ratio Midbrainlceret,mm ratio
Controls (n = II)
Anorectics (n -- 12)
Bulimics (n = 12)
27.8 - 6 (21.0-39.0) 122.6 -4- 13 (108.0-150.0) 5.9 -- 0.9 (4.4--7.6) 7.5 ± 0.4 (6.7-8.1) 0.7 ± 0.1 (0.5-1.0) 2 6 ± 1.3 (I.3--6.0) !.9 - 0.4 (I.4-2.9) 2.5 ± 0.4 (2.1-3.3) 5.1 ~ 0.4 (4.4-5.6) 0.9 ± 0.2 (0.7-1.3) 0.012 - 0.002 (0.008-0.0157) 0.015 - 0.002 (0,011-0,02)
25.3 - 7.0 (17.0--42.0) 89.3 - 14.6 (68.0-110.0) 5.4 ± 0.9 (4.2-7.1) 7.2 - 0.4 (6.6-7.7) 0.6 ± 0.1 (0.4-0.8) 2.7 - 1.0 (1.3--4.9) 1.4 .+ 0.5 (0.3-2.2) 2.2 ± 0.4 (1.6-2.6) 5.0 ± 0.5 (4.2-5.7) 0,8 ~" 0.1 (0.6--I.0) 0.0088 4. 0.0034 (0.0018-0.0143) 0,013 ± 0.001 (0.001-0,0154)
24.5 - 4.0 (18.0-34.0) 134.2 .4- 12 (H0.0--187.0) 5.9 "4- 0.7 (4.8-7.1) 7.3 ± 0.5 (6.6-8.2) 0.6 ± 0,1 (0.6-0.8) 2.4 ± 1.4 (1.4--6.3) i.9 4. 0.4 (1.0-2.5) 2.5 ± 0.2 (2.0-2.8) 5.0 ± 0.4 (4.0-6.0) 0.8 ± 0.2 (0.6-1.2) 0.012 ± 0.0025 (0.0058-0.016) 0.015 ± 0.001 (0,0134--0,0174)
All data shown are mean 4. SD (range). C.C, = corpus callosum, sep pel = septum pellucidum.
Table 2. Results of ANOVA Comparing Midsaggital Areas among Anorectics, Bulimics, and Controls
Cerebrum C . C . area C . C . length C . C . width Sep pel
Thalamus Midbrain Pons IVth vent
F
p
!.39 1.25 0.80 !.87 0.18 4.88 4.47 0.21 !.78
026 0.30 0.45 0.17 0.83 0.01 ° 0.01 ° 0.81 0.18
Post hoc (p < 0.05)
AvsB, AvsC AvsB, AvsC
Abbreviations: A = anorectics, B = bulimics, C = Controls. ~Significant.
Discussion Thalamus and midbrain were the two structures where significant changes were noted in patients with anorexia nervosa. Both the thalamus and midhrain were smaller in anorectic patients, but not in bulimics or controls. Although the thalamus is not classically considered to regulate eating behaviors (Guyton 1989), remarkable improvement was reported in a single case of severe anorexia nervosa following stereotaxic lesions of the right dorsomedial and intralaminar thalamic nuclei (D'Andrea et al 1974). Further, the thalamus is a part of the basal ganglia circuit,
the same circuit in which metabolic abnormalities have been noted on PET scans (Herholz et al 1987). These findings are in agreement with Wu et al's report (1990) demonstrating lack of changes in the basal ganglia in patients with bulimia. It is thus possible that the neuronal circuits involved in these two disordera may be different. The role of the midbrain and reasons for differences in size are unclear. It is possible that the dopamine neurons in the midbrain may be affected in anorexia but further studies are needed to examine this hypothesis. The role of monoamines has not been well studied, however, a recent report by Sato et al (1988) demonstrating a marked reduction in dopamine excretion in anorexia nervosa lends support to this notion. In conclusion, this study suggests that focal brain abnormalities may be involved in the etiology or manifestations of anorexia nervosa.
References ArtmannH, Gran H, AdelmannM, Schleiffer (1985): Reversible and non-reversible enlargement of cerebrospinal fluid spaces in anorexia nervosa. Neuroradiology 27:304-312. Brant-Zawaldski M, Norman D (1987): Magnetic Resonance Imaging of the Central Nervous System. New York: Raven Press. D'Andrea F, De Devitiis E, Megna G, De Giacomo
738
BIOLPSYCHIATRY 1992;31:735-738
Brief Reports
P, Pietri G (1974): Remissione de anoressia men- Hoffman GW, Ellinwood EH Jr, Rockwell WJ, Hefttale resistente ad aitre terapie in seguito a lalakins RJ, Nishita JK, Gutherie LF (1989b): Cemolisi stereotassia [Remission of treatment-rerebral atrophy in bulimia. BiolPsychiatry 25:894sistant anorexia nervosa following stereotaxic 902. thalamotomy]. Riv Patol Nerv Ment 95:579-590. Hoffman GW, Ellinwood EH Jr, Rockwell WJ, HeftDoraiswamyPM, KrishnanKR, Figiel GS, et al (1990): kins RJ, Nishita JK, Gutherie Lt~ (1990): Brain A brain MRI study of pituitary gland morphology T! measured by magnetic resonance imaging in in anorexia nervosa and bulimia. Biol Psychiatry bulimia. Biol Psychiatry 27:116-119. 28:110-116. Krieg JC, Backmund H, Pirke KM (1986): Endocrine Doraiswamy PM, Krishnan KR, Boyko OB, et al metabolic, and brain morphological abnormalities (1991): Pituitary abnormalities in eating disorders. in patients with eating disorders, lnt J Eating DisProg Neuropsychopharmacol Biol Psychiatry orders 5:999-1005. 15:351-356. Krieg JC, Pirke KM, Lauer C, Backmund H (1988): Enzmann DR, La~e B (1977): Cranial computed toEndocrine, metabolic, and cranial computed tommography findings in anorexia nervosa. J Comput ographic findings in anorexia nervosa. Biol PsyAssist Tomogr 1(4):410-414. chiatry 23:377-387. Guyton AC (1989): Textbook of Medical Physiology. Krieg JC, Lauer C, Leinsinger G, et al (1989a): Brain Philadelphia: W.B. Saunders Co., p. 863. morphology and regional cerebral blood flow in anorexia nervosa. Biol Psychiatry 25:1041-1048. Heinz ER, Martine J, Haenggeli A (1977): Reversibility of cerebral atrophy in anorexia nervosa and Krieg JC, Lauer C, Pirke KM (1989b): Structural Cushing's syndrome. J Comput Assist Tomogr brain abnormalities in patients with bulimia nero 1(4):415-418. rosa. Psychiatry Res 27:39-48. Herholz K, Krieg JC, Emrich HM, et al (1987): Re- Sato T, Igarashi N, Miyagawa K, Nakajima T, Kagional cerebral glucose metabolism in anorexia tayoma T (1988): Catecholamine and thyroid menervosa measured by positron emission tomogtabolism in a case of anorexia nervosa endocriraphy. Biol Psychiatry 22:43-51. nology: Japonica 35:295-301. Hoffman GW, Eilinwood EH Jr, Rockwell WJ, Heft- Wu J, Hagman,i, Buchsbaum MS, et al (1990): Greater kins RJ, Nishita JK, Gutherie LF (1989a): Celeft cerebral hemispheric metabolism in bulimia rebral atrophy in anorexia nervosa: A pilot study. assessed by positron human tomography. Am J Biol Psychiatry 26:321-324. Psychiatry 47:309-329.
"735
BRIEF REPORTS
Subcorticai Brain Anatomy in Anorexia and Bulimia Mustafa M. Husain, Kevin J. Black, P. Murali Doraiswamy, Sunjay A. Shah, W. J. Kenneth Rockwell, Everett H. Ellinwood, Jr., and K. Ranga Rama Krishnan
Introduction Many studies have reported a generalized decrease in brain volume ("pseudoatrophy") in patients with anorexia nervosa and bulimia (Enzmann and Lane 1977; Heinz et al 1977; Hoffman et al 1989a and b; Krieg et al 1989b). To some degree this change is reversible, but some enlargement of cerebrospinal fluid (CSF) spaces appears to persist despite normalization of weight and eating habits (Artmann et al 1985; Krieg et al 1986, 1988). Change that persists after successful treatment might be due to residual damage to the brain or persistent abnormal metabolism; however, it might also represent underdeveloped or involuted areas that were originally responsible for the behavioral pathology (Artmann et al 1985). However, previous in vivo anatomic studies have focused only on the gross finding of CSF space enlargement or have used techniques with poor spatial resolution and partial voluming problems (i.e., single photon emission computed tomography (SPECT); Krieg et al 1989a). Limited studies of regional cerebral metabolism have shown focal changes: one small positron From the Department of Psychiatry, Duke University Medical Center, Durham. NC (MMH, PMD. WJKR, EHE, KRRK), Washington University School of Medicine. St. Louis, MO (KIB). School of Medicine, U "ive~;ty of North Carolina. Chapel Hill, NC (SAS), and University of Texas Southwestern Medical School, Dallas, TX (MMH). Address reprint requests to Dr. Everett H. Ellinwood. Department of Psychiatry, Box 3870, Duke University MeJical Center, Durham, NC 27710. Received May 20, 1991; revised November I, 1991.
© 1992 Society of Biological Psychiatry
emission tomography (PET) study of anorexia (Herholz et ai 1987) suggested focal metabolic abnormalities in the striatum, tempotal cortex, thalamus, and brainstem; and a study comparing magnetic resonance imaging (MRI) Tt values in bulimics and controls found a significant difference in the inferior frontal lobe, but not in other brain regions surveyed (Hoffman et al 1990). Because Herholz et al have reported focal metabolic abnormalities in the basal ganglia we decided to assess changes in midline subcortical structures and brainstem in patients with eating disorder.
Methods
Subjects Patients were 24 women undergoing treatment at the Duke University Medical Center Eating Disorders Unit, who had received diagnoses of anorexia nervosa (n = 12) or bulimia (n = 12) by DSM-III criteria. Average age was 25.3 .47 years (SD) for anorectics and 24.5 __ 4 years for bulimics. One of the anorectic patients had a bingeing episode. None of the bulimics had a past history of anorexia nervosa. Four of the 12 bulimic and 11 of the 12 anorectic patients had menstrual dysfunction. The average duration of the illness in bulimics was 88.7 __ 45 months. The average duration of the illness in anorectics was 62.7 _ 52.36 months. Controls were 11 normal subjects screened 0006-3223/92/$05.00
736
Brief Reports
BIOLPSYCHIATRY 1992;31:735-738
for psychiatric disorders. Average age for controis was 27.8 ___ 6 years. Clinical characteristics of these subjects have been described previously (Doraiswamy et al 1990, 1991). The weight (lbs)/height (kiches) ratio for anorectics (1.41 -_. 0.24) was smaller than for controls (1.88 ± 0.14)and bulimics (2.04 --+ 0.36) (F = 13.59, df = 2, p < 0.0001). Post hoe testing confirmed this finding.
Image Acquisition MRI was performed on a 1.5 Tesla General Electric (Milwaukee, Wl). Scans were performed with the subject's head positioned with the canthomeatal line at zero degrees from the vertical axis and the imager's grid centered at the nasion. Midsagittal T~ weighted images were selected as previously described (Doraiswamy et al 1990). Scans that did not result in a midline image (failed to demonstrate the cerebral aqueduct) or did not contain the entire intracranial area in the scanning window were not included in the study.
Image Analysis The following cross-sectional area and distance measurements were performed on each midsagittal scan: corpus callosum (length, width, and area); cerebral cortex (,area); septum peilucidum (area); thalamus (area); fourth ventricle (area); midbrain and pens (areas). The areas were defined using a standard MRi atlas (Brant-Zawadski Man, t Norman D 1987). Regions of interest were traced and measured using standard Signa offline software (Doraiswamy et al 1990). Midbrain asse~Isment was made using a standard MRI atlas (Brant-Zawadski M and Norman D 1987). The upper extent of the colliculi was used to determine the upper border and the bulge of the pens t~determine the lower border of the midbrain. All tracings were conducted blind to the diagnosis. Corpas callosum (CC) measurements were chosen relative to the longest (A-P) axis, starting from the most anterior and most posterior reaches of the internal (inferior)border
of the CC. The "middle" thickness was measured perpendicular to the longest axis at a point halfway between the anterior and posterior poles of the CC.
Statistical Methods Data were analyzed using PC-SAS (SAS Institute, Cary, NC). Group comparisons were made with analysis of variance (ANOVA) and post hoe tests; and correlation between variables was assessed with Pearson's Correlation Coefficient. Normality of distribution was assessed using Shapiro Wilk statistic and when the assumption was not satisfied, nonparamelric tests were used.
Results There was no significant difference in age of subjects by diagnosis. Table l summarizes the measurements of different midsagittal brain structures in all three groups. The most significant finding in this study was the smaller thalamus area in anorectic (1.4 __ 0.5 cm2) patients as compared with bulimics (1.9 -+ I cm 2) and controls (I.93 ± 0.4 cm 2) (F -- 4.88, p = 0.01). These differences were confirmed by post hoc tests. The midbrain area was also significantly smaller in anorectic (2.17 -+ 0.35 cm 2) patients as compared with bulimics (2.48 __ 0.23 cm2) and controls (2.54 ± 0.35 cm2) (F - 4.47, p - 0.01)(see Table 2). Bulimics did not differ from controls. The anorectic who also had bingeing did not differ from the other anorectic patients. There was no correlation between body weight, duration of illness, thalamus, and midbrain. The ratio of the thalamus/cerebral hemisphere, were significantly different between patients and controls ( F = 4.06, df -- 2, p < 0.04). The significance was due to differences between anorectics and controls. The ratio of the midbrain/cerebral hemisphere was also different between p,ttients and controls (F = 19.3, df -- 2, p < 0.0001). The differences were confirmed by post hoc tests to be due to the anorectic subjects.
Brief Reports
n10LPSYCHIATRY
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1992 ;31:735 -738
Table !. MRI Measurements in Anorectics, Bulimics, and Controls
Age (yr) Weight (Ibs) C.C. area (era 2) C,C. length (cm) C.C. widlh (cm) Sep Pel (cm") Thalamus (cm') Midbruin (cm') Ports (cm2) IVth vent (cm~)
Thalamus/cerebrum ratio Midbrainlceret,mm ratio
Controls (n = II)
Anorectics (n -- 12)
Bulimics (n = 12)
27.8 - 6 (21.0-39.0) 122.6 -4- 13 (108.0-150.0) 5.9 -- 0.9 (4.4--7.6) 7.5 ± 0.4 (6.7-8.1) 0.7 ± 0.1 (0.5-1.0) 2 6 ± 1.3 (I.3--6.0) !.9 - 0.4 (I.4-2.9) 2.5 ± 0.4 (2.1-3.3) 5.1 ~ 0.4 (4.4-5.6) 0.9 ± 0.2 (0.7-1.3) 0.012 - 0.002 (0.008-0.0157) 0.015 - 0.002 (0,011-0,02)
25.3 - 7.0 (17.0--42.0) 89.3 - 14.6 (68.0-110.0) 5.4 ± 0.9 (4.2-7.1) 7.2 - 0.4 (6.6-7.7) 0.6 ± 0.1 (0.4-0.8) 2.7 - 1.0 (1.3--4.9) 1.4 .+ 0.5 (0.3-2.2) 2.2 ± 0.4 (1.6-2.6) 5.0 ± 0.5 (4.2-5.7) 0,8 ~" 0.1 (0.6--I.0) 0.0088 4. 0.0034 (0.0018-0.0143) 0,013 ± 0.001 (0.001-0,0154)
24.5 - 4.0 (18.0-34.0) 134.2 .4- 12 (H0.0--187.0) 5.9 "4- 0.7 (4.8-7.1) 7.3 ± 0.5 (6.6-8.2) 0.6 ± 0,1 (0.6-0.8) 2.4 ± 1.4 (1.4--6.3) i.9 4. 0.4 (1.0-2.5) 2.5 ± 0.2 (2.0-2.8) 5.0 ± 0.4 (4.0-6.0) 0.8 ± 0.2 (0.6-1.2) 0.012 ± 0.0025 (0.0058-0.016) 0.015 ± 0.001 (0,0134--0,0174)
All data shown are mean 4. SD (range). C.C, = corpus callosum, sep pel = septum pellucidum.
Table 2. Results of ANOVA Comparing Midsaggital Areas among Anorectics, Bulimics, and Controls
Cerebrum C . C . area C . C . length C . C . width Sep pel
Thalamus Midbrain Pons IVth vent
F
p
!.39 1.25 0.80 !.87 0.18 4.88 4.47 0.21 !.78
026 0.30 0.45 0.17 0.83 0.01 ° 0.01 ° 0.81 0.18
Post hoc (p < 0.05)
AvsB, AvsC AvsB, AvsC
Abbreviations: A = anorectics, B = bulimics, C = Controls. ~Significant.
Discussion Thalamus and midbrain were the two structures where significant changes were noted in patients with anorexia nervosa. Both the thalamus and midhrain were smaller in anorectic patients, but not in bulimics or controls. Although the thalamus is not classically considered to regulate eating behaviors (Guyton 1989), remarkable improvement was reported in a single case of severe anorexia nervosa following stereotaxic lesions of the right dorsomedial and intralaminar thalamic nuclei (D'Andrea et al 1974). Further, the thalamus is a part of the basal ganglia circuit,
the same circuit in which metabolic abnormalities have been noted on PET scans (Herholz et al 1987). These findings are in agreement with Wu et al's report (1990) demonstrating lack of changes in the basal ganglia in patients with bulimia. It is thus possible that the neuronal circuits involved in these two disordera may be different. The role of the midbrain and reasons for differences in size are unclear. It is possible that the dopamine neurons in the midbrain may be affected in anorexia but further studies are needed to examine this hypothesis. The role of monoamines has not been well studied, however, a recent report by Sato et al (1988) demonstrating a marked reduction in dopamine excretion in anorexia nervosa lends support to this notion. In conclusion, this study suggests that focal brain abnormalities may be involved in the etiology or manifestations of anorexia nervosa.
References ArtmannH, Gran H, AdelmannM, Schleiffer (1985): Reversible and non-reversible enlargement of cerebrospinal fluid spaces in anorexia nervosa. Neuroradiology 27:304-312. Brant-Zawaldski M, Norman D (1987): Magnetic Resonance Imaging of the Central Nervous System. New York: Raven Press. D'Andrea F, De Devitiis E, Megna G, De Giacomo
738
BIOLPSYCHIATRY 1992;31:735-738
Brief Reports
P, Pietri G (1974): Remissione de anoressia men- Hoffman GW, Ellinwood EH Jr, Rockwell WJ, Hefttale resistente ad aitre terapie in seguito a lalakins RJ, Nishita JK, Gutherie LF (1989b): Cemolisi stereotassia [Remission of treatment-rerebral atrophy in bulimia. BiolPsychiatry 25:894sistant anorexia nervosa following stereotaxic 902. thalamotomy]. Riv Patol Nerv Ment 95:579-590. Hoffman GW, Ellinwood EH Jr, Rockwell WJ, HeftDoraiswamyPM, KrishnanKR, Figiel GS, et al (1990): kins RJ, Nishita JK, Gutherie Lt~ (1990): Brain A brain MRI study of pituitary gland morphology T! measured by magnetic resonance imaging in in anorexia nervosa and bulimia. Biol Psychiatry bulimia. Biol Psychiatry 27:116-119. 28:110-116. Krieg JC, Backmund H, Pirke KM (1986): Endocrine Doraiswamy PM, Krishnan KR, Boyko OB, et al metabolic, and brain morphological abnormalities (1991): Pituitary abnormalities in eating disorders. in patients with eating disorders, lnt J Eating DisProg Neuropsychopharmacol Biol Psychiatry orders 5:999-1005. 15:351-356. Krieg JC, Pirke KM, Lauer C, Backmund H (1988): Enzmann DR, La~e B (1977): Cranial computed toEndocrine, metabolic, and cranial computed tommography findings in anorexia nervosa. J Comput ographic findings in anorexia nervosa. Biol PsyAssist Tomogr 1(4):410-414. chiatry 23:377-387. Guyton AC (1989): Textbook of Medical Physiology. Krieg JC, Lauer C, Leinsinger G, et al (1989a): Brain Philadelphia: W.B. Saunders Co., p. 863. morphology and regional cerebral blood flow in anorexia nervosa. Biol Psychiatry 25:1041-1048. Heinz ER, Martine J, Haenggeli A (1977): Reversibility of cerebral atrophy in anorexia nervosa and Krieg JC, Lauer C, Pirke KM (1989b): Structural Cushing's syndrome. J Comput Assist Tomogr brain abnormalities in patients with bulimia nero 1(4):415-418. rosa. Psychiatry Res 27:39-48. Herholz K, Krieg JC, Emrich HM, et al (1987): Re- Sato T, Igarashi N, Miyagawa K, Nakajima T, Kagional cerebral glucose metabolism in anorexia tayoma T (1988): Catecholamine and thyroid menervosa measured by positron emission tomogtabolism in a case of anorexia nervosa endocriraphy. Biol Psychiatry 22:43-51. nology: Japonica 35:295-301. Hoffman GW, Eilinwood EH Jr, Rockwell WJ, Heft- Wu J, Hagman,i, Buchsbaum MS, et al (1990): Greater kins RJ, Nishita JK, Gutherie LF (1989a): Celeft cerebral hemispheric metabolism in bulimia rebral atrophy in anorexia nervosa: A pilot study. assessed by positron human tomography. Am J Biol Psychiatry 26:321-324. Psychiatry 47:309-329.
