Tim Crow

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Template:Cleanup-date Professor Tim Crow is a British psychiatrist and researcher. Much of his research is related to the causes of schizophrenia. He serves as Honorary Director of the Prince of Wales International Centre for Research into Schizophrenia and Depression.

Tim Crow is a research psychiatrist who is Director of the Prince of Wales SANE Research Centre. He qualified at the Royal London Hospital in 1964 and obtained a PhD in the University of Aberdeen, Scotland, in 1970. He is a fellow of the Royal Colleges of Physicians and Psychiatrists and the Academy of Medical Sciences. Professor Crow was for twenty years Head of the Division of Psychiatry of the MRC Clinical Research Centre at Northwick Park and then a member of the External Scientific staff of the Medical Research Council in Oxford.

Tim Crow’s long term research interests are in the nature and causation of the major psychoses. These illnesses are characterised by the presence of delusions and hallucinations and disorders of thinking and generally have an onset in early and middle adult life. Encompassing schizophrenia and manic-depressive psychosis these disorders are common, affecting around 2% of the population in the course of a lifetime.

In the first CT scan study in 1976 Professor Crow and colleagues at Northwick Park demonstrated that there are structural changes (eg a degree of enlargement of the cerebral ventricles) in individuals who have suffered from schizophrenia. Much subsequent work with MRI scans and in post-mortem brain studies has confirmed this and suggests that the changes are in the cerebral cortex and particularly are related to the subtle asymmetries that are characteristic of the human cortex.

What is the origin of these changes? In earlier work Professor Crow considered but was able to rule out a viral causation. There is a genetic component but the nature has been obscure. Professor Crow’s particular recent contribution has been the proposal that the origins of the psychoses relate particularly to those characteristics eg cerebral asymmetry that are associated with the specifically human capacity for language. This leads to a theory of the origin of psychotic symptoms – that they are associated with deviations in the subtle asymmetries of development of the cortex, and that the symptoms arise as confusions between thought and speech and through the abnormal attachment of meaning to perceived speech – and to its genetic basis in the change that led to the evolution of Homo sapiens as a species.

The work of the Prince of Wales Centre will focus on this theory through 1) radiological investigations of brain structure in relation to the symptoms of psychosis, 2) post-mortem studies of the nature of the change at a cellular level, and 3) investigation of a gene (ProtocadherinXY) located on the X and Y chromosomes that has changed in the course of hominid evolution and may have played a particular role in the development of the cerebral cortex, and the evolution of language and the origins of psychosis.

CURRENT CONTENTS CITATION CLASSICS 1) Crow TJ. (1972) Catecholamine-containing neurones and electrical self-stimulation 1 A review of some data. Psychological Medicine 3: 66-73 nominated on 28 December 1981 with 115 citations

II) Crow TJ. (1980) Molecular pathology of schizophrenia; more than one disease process? Brit Med J 280: 66-68 nominated on 29 November 1993 with 585 citations

MOST FREQUENTLY CITED PAPERS: (SCI citations Oct 2005) 1) Sole author papers:

i) Molecular pathology of schizophrenia; more than one disease process?

    Brit Med J 1980; 280: 66-68. (1264 citations)						

ii) The two syndrome concept: origins and current status.

    Schiz Bull 1985; 11: 471-486.(472 citations)

iii) Temporal lobe asymmetries as the key to the etiology of schizophrenia.

    Schiz Bull 1990; 16: 433-443.(275 citations)

iv) Positive and negative schizophrenic symptoms and the role of dopamine.

    Brit J Psychiatry 1980; 137: 383-386 (222 citations)

v) The continuum of psychosis and its implication for the structure of

    the gene.   
    Brit J Psychiat 1986; 149: 419-429(187 citations)

vi) A map of the rat mesencephalon for electrical self-stimulation

    Brain Research 1972;  36: 265-273    (184 citations)

vii) Catecholamine-containing neurones and electrical self-stimulation:

    I a review of some data.  Psychol Med 1972; 2: 414-421(152 citations)

viii)A re-evaluation of the viral hypothesis: is psychosis due to retroviral

    integration at the site of the cerebral dominance gene?  
    Brit J Psychiat 1984; 145: 243-253 (136 citations)			      	   

ix) Schizophrenia as failure of hemispheric dominance for language.

    Trends in Neurosci 1997; 20: 339-343  (120 citations)

x) Sex chromosomes and psychosis: the case for a pseudo-autosomal locus.

    Brit J Psychiatry 1988; 153: 675-683 (120 citations)						

xi) Cortical synapses and reinforcement: an hypothesis.

    Nature 1968; 219: 736-737	(107 citations)

xii) Sexual selection, Machiavellian intelligence and the origins of

    psychosis. Lancet 1993; 342: 594-598  (106 citations)

xiii)The continuum of psychosis and its genetic origins.

    The Sixty-fifth Maudsley Lecture.  
    Brit J Psychiat 1990; 156:788-797(100 citations)

2) First authored papers: i) Crow TJ et al. Schizophrenia as an anomaly of development of

    cerebral asymmetry: a post-mortem study and a proposal concerning the 
    genetic basis of the disease.   
    Arch Gen Psychiatry 1989; 46: 1145-1150 (323 citations)

ii) Crow TJ et al. Neurotransmitter receptors and monoamine metabolites

    in the brains of patients with Alzheimer-type dementia and depression, 
    and suicides.       
    Neuropharmacology 1984; 23: 1561-1569 (246 citations)

iii) Crow TJ et al. The Northwick Park study of first episodes of schizophrenia:

    a randomized controlled trial of prophylactic neuroleptic treatment
    Brit J Psychiat 1986; 148: 120-127.(212 citations)

iv) Crow TJ et al. Monoamine mechanisms in chronic schizophrenia;

    post-mortem neurochemical findings. 
    Brit J Psychiatry 1979; 134: 249-256(179 citations)

v) Crow TJ, Spear PJ, Arbuthnott GW. Intracranial self-stimulation with

    electrodes in the region of the locus coeruleus. 
    Brain Research 1972; 36: 275-283.(177 citations)

3) Co-authored papers: i) Allen YS et al. Neuropeptide Y distribution in the rat brain.

    Science 1983; 221: 877-879 (828 citations)

ii) Johnstone EC et al. Cerebral ventricular size and cognitive impairment

    in chronic schizophrenia. 
    Lancet 1976; ii: 924-926	(629 citations)

iii) Hsiao K et al. Linkage of a prion protein mis-sense variant to

    Gerstmann-Straüssler syndrome.    Nature 1989: 338: 342-345.								                          (535 citations)

iv) Brown R et al. Post-mortem evidence of structural brain changes in

    schizophrenia.      
    Arch Gen Psychiatry 1986; 43: 36-42(527 citations)

v) Adrian TE et al. Neuropeptide Y: distribution in human brain.

    Nature 1983; 306: 584-586(482 citations)							    

vi) Owen F et al. Increased dopamine receptor sensitivity in schizophrenia.

    Lancet 1978; ii: 223-226(416 citations)