Neurodevelopmental Aspects of Bipolar Affective Disorder Over the past decade most of the structural brain abnormalities in schizophrenia on CT and MRI scans have also been found in bipolar affective disorder. These include lateral and third ventricular enlargement, cortical sulcal and fissure widening, and cerebellar atrophy (Nasrallah et al, 1989). Yet, while these structural brain findings have been regarded as an integral part of the evidence for a neurodevelopmental etiological process in schizophrenia (Lewis and Murray, 1987; Nasrallah, 1990; Weinberger, 1987), no such claims have been made for bipolar disorder. Two recent MRI findings, however, support a neurodevelopmental etiology for bipolar disorder, similar to schizophrenia: 1. The frequency of medial temporal lobe (hippocampus/amygdala complex) hypoplasia in bipolar disorder is about the same as that found in schizophrenia (Olson et al, 1990). 2. Total cerebral volume is significantly reduced in both schizophrenia and bipolar disorder compared with controls (NasraUah et al, 1990). Those two findings suggest the possibility that a disruption of brain development could contribute to bipolar disorder. A smaller cerebrum may be a result of first trimester (proliferative) impairment, or a perinatal (hypoxic) insult to the developed cerebrum in • e third trimester. The hypoplastic medial temporal lobe in some bipolar patients may reflect a second trimester disruption of hippocampal development. Another line of evidence for a possible nemodevelopmental process in bipolar disorder is the lack of progressive increase in cerebral vestibular size over time. Follow-up studies of ventricular size in schizophrenia have suggested a static (developmental) rather than a progressive (degenerative) lesion (Nasrallah et al, 1986; Illowsky et al, 1988; Vita et al, 1988). One published follow-up study of bipolar patients also indicates an absence of progressive ventricular enlargement (Woods et al, 1990). However, some recent data suggest that there is progression in cerebral ventricular size in at least a subgroup of schizophrenic patients early in the illnzss (Kemali et al, 1989; DeLisi et al, 1990). Neuropathologic studies have been pursued far more extensively in schizophrenia than in bipolar disorder. Too little gliosis has been found in schizophrenic brains to indicate a neurodevelopmental lesion (Roberts et al, 1990). Several recent histoarch;.~ec~ral findings suggest disrupted neuronal migration or elimination in certain brain areas (e.specially temporo-limbic) in schizophrenia (Nasrallah, 1990). Similar studies in bipolar disorder will be necessary to lend further support to a neurodevelopmental model. Excessive perinatal complications have been frequently reported in schizophrenia, but not adequately studied in bipolar disorder (Lewis and Murray, 1987; Schwarzkopf et al, 1989). Several studies have found an association betweeu obstetric complications and ventriculomegaly in schizophrenia (Murray et al, 1988), but there are no similar studies in bipolar disorder. Crow (1990) has proposed that schizophrenia and affective disorder are part of a © 1991 Society of Biological Psychiatry




continuum, and that attempts to draw a "genetic line of demarcation" between them have failed. It could be said that studies of brain structure have also failed to distinguish between those two disorders, it is possible that there are areas of overlap in the etiology of schizophrenia and bipolar disorder, and that neurodevelopmental processes, including a disruption of gene expression of brain growth and sculpture, are part of the overlap. It is important in future studies to conduct the same neurobiological research simultaneously in schizophrenia and bipolar disorder and to compare both to a healthy control group in order to detect what is specific and what is common in those two disorders. The data so far suggest that like schizophrenia, bipolar disorder has neurodevelopmental correlates that deserve further investigation. Henry A. Nasrallah References Crow TJ (1990): The continuum of psychosis and its genetic origins. Br J Psychiatry 156:788797. DeLisi LE, Hoff A, Shields G, Schwarz J, Halthore S, Anand A (1990): Brain morphology in first episode cases of schizophrenia. Abstracts of the 17th Congress of Collegium lnternationale Neuro-Psychopharmacoloqium, September 10-14, Kyoto, Japan, Volume II, p 239. lllowsky BP, JulianoDM, BigelowLB, WeinbergerDR (1988): Stabilityof CT scan findingsin schizophrenia: Results of an 8-yearfollow up study. JNeurolNeurosurg Psychiatry 51:209-213. Kemali D, Maj M, Galderisi S, Milici N, Salvati A (1989): Ventricle-to-brainratio in schizophrenia: A controlled follow up study. Biol Psychiatry 26:753-756. Lewis SW, Murray RM (1987): Obstetric complications, neurodevelopmental deviance and risk of schizophrenia, d Psychiat Res 21:413-421. Murray RM, Reveley AM, Lewis SW (1988): Family history, obstetric complications and cerebral abnormality in schizophrenia. In: The Handbook of Schizophrenia Volume 3: Nosology, Epidemiology, and Genetics of Schizophrenia (M.T. Tsuang and J,C. Simpson, eds). Elsevier, Amsterdam, pp 563-577. Nasrallah HA (1990): Brain structure and functions in schizophrenia: Evidence for fetal neurodevelopmental impairment. Curr Opin Psych 3: 75-78. Nasrallah HA, Coffman JA, Olson SC (1989): Structural brain imaging findings in affective disorders: An overview. J Neuropsychiat Clin Neurosci 1:21-26. Nasrallah HA, Olson SC, McCalley-Whitters M, Chapman S, Jacoby CG (1986): Cerebral ventricular enlargement in schizophrenia: A preliminary follow up study. Arch Gen Psychiatry 43:157-159. Nasrallah HA, Olson SC, Schwarzkopf SB (1990): Diminished brain volume in bipolar disorder. Paper presented at the Annual Meeting of the American College of Neuropsychopharmacology, December 10-15, San Juan, Puerto Rico. Olson SC, Bogerts B, Coffman JA, Schwarzkopf SB, Nasrallah HA (1990): Medial-temporal and ventricular abnormalities by MRI: Comparing major psychoses. Biol Psychiatry 27:59A-60A. Roberts GW, Bruton CJ (1990): Notes from the graveyard: Neuropathology and schizophrenia. Neuropathol App Neurobiol 16:3-16. Schwarzkopf SB, Nasrallah HA, Olson SC, Coffman JA, McLaughlin JA (1989): Perinatal complications and genetic loading in schizophrenia: Preliminary findings. Psychiatry Res 27:233-239. Vita A, Sacchetti E, Valvassori G, Cazzullo L (1988): Brain morphology in schizophrenia: A 25 year CT scan follow up study. Acta Psychiatr Scand 78:618-621. Weinberger DR (1987): Implications of normal brain development for the pathogenesis of schizophrenia. Arch Gen Psychiatry 44:660-669. Woods BT, Yurgelum-Todd, Benes FM, Frankenberg FR, Pope HG, McSparren J (1990): Progressive ventricular enlargement in schizophrenia: Comparison to bipolar affective disorder and correlation with clinical course. Biol Psychiatry 27:341-352.

Neurodevelopmental aspects of bipolar affective disorder.

BIOL PSYCHIATRY 1991;29:1-2 EDITORIAL Neurodevelopmental Aspects of Bipolar Affective Disorder Over the past decade most of the structural brain abn...
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