Observations on the Histopathology of Schizophrenia

Winkelman, N. W.; Book, Marius

doi:10.1176/ajp.105.12.889

Cited by 39 publications

(16 citation statements)

References 17 publications

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“…In der vergleichsweise jungen Geschichte der biologischen Psychiatrie haben neuropathologische Untersuchungen die älteste und wohl kontroversenreichste Tradition. In der ersten Hälfte dieses Jahrhunderts erschienen mehr als 250 neuropathologische Untersuchungen an Gehirnen Schizophrener (Literaturübersichten: 14,15,56,62,67,89,91). Namhafte Beftirworter eines neuropathologischen Substrates schizophrener Erkrankungen waren die Vogts und deren Mitarbeiter, nach deren Auffassung vorwiegend im Tha-lamus und Neokortex Schizophrener sogenannte "Schwundzellen" (gekennzeichnet durch eigenartige Zytoplasmaauflösungen bei relativ gut erhaltenem Zellkern) und "Lückenfelder" (bedingt durch fokale NervenzellausHille) anzutreffen waren (3,23,32,34,84,85).…”

Section: Introductionunclassified

Zur Neuropathologie der Schizophrenien

Bogerts¹

1984

Fortschr Neurol Psychiatr

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Up to now it is not known whether the ventricular enlargement in schizophrenics demonstrated by neuroradiological investigations is caused by a general brain atrophy or a more or less selective degeneration of one or several areas. Therefore, the volumes of several parts of the basal ganglia, of the diencephalon and of the limbic system were determined by planimetry of myelin-stained serial sections in post mortem brains of 14 schizophrenic patients and 13 control cases. The important limbic structures of the temporal lobe (amygdala, hippocampal formation), the ventricle closely surrounding structures of the diencephalon, and the pallidum internum are significantly smaller in the schizophrenic group, whereas the volumes of the pallidum externum, of the three parts of the striatum (caudatum, putamen, n. accumbens), of the red nucleus, and of the large thalamic cell groups have not significantly changes. The volume reductions are interpreted as focal degenerative shrinkages of unknown etiology.

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Section: Introductionunclassified

Zur Neuropathologie der Schizophrenien

Bogerts¹

1984

Fortschr Neurol Psychiatr

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“…Inasmuch as it is unlikely that each of the pathologies presented in TABLES 2 and 3 represents a separate cause of schizophrenia, a major question is how many of these individual brains demonstrate significant deviations from the norm in more 69 Not found 70 Abnormal orientation of neurons 71 Not found 70,72 Decreased MAP 2, 5, in hippocampal subfields 73 Decreased synaptophysin mRNA 74 Decreased Glu R1 Glu R2 75 Entorhinal cortex: Abnormal architecture in 40% of cases 76,77 Not found 78 Thalamus: Decreased neurons in mediodorsal nucleus 79,80 Prefrontal and cingulate cortex: Upregulation of GABA A receptor binding 81,82 Decreased small neuron density 83 Increased neuron density 84 No change 88 Increased vertical axons cingulate cortex 86 Decreased GAD gene expression 85 Abnormal migration of NADPH cells 87,88 Association cortex: Increased GAP- 43 89 Gliosis: Periventricular, periaqueductal, subcortical 4,90,91 No glial increase in cortex, brain stem, thalamus, limbic structures 51,91,92 None in "purified" sample 53 Fibrin degradation products increased: possible marker for inflammation 93 than one domain. Unfortunately, few laboratories can conduct more than one or two assays in the same areas of the same brains.…”

Section: The Neuropathologies Of Schizophreniamentioning

confidence: 99%

Epilepsy, Schizophrenia, and the Extended Amygdala

Stevens

1999

Annals of the New York Academy of Sciences

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Propagation and prolongation of rapid neuronal discharge underlies the epilepsies. However, episodic focal rapid neuronal discharges limited to discrete nuclei and pathways of the amygdala-hippocampal-septal-hypothalamic networks are the language of physiologic message systems for endocrine regulation and reproductive activities vital to the survival of the organism and the species. To prevent prolongation and propagation of physiologic pulsed excitation to areas outside specific networks and resultant epileptic seizures, these discharges must be limited in extent and time by powerful inhibitory processes. The nucleus accumbens, a unit of the extended amygdala, and the monoamines and GABA are components of the inhibitory networks that restrict physiologic rapid discharge in duration and in location. In parallel to the relationship of excessive neuronal excitation to epilepsy, evidence will be presented that excessive inhibition via one or more components of these inhibitory networks or diminished excitation underlies development of some psychoses, including schizophrenia.

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“…While many investigators believed that there was ample evidence to support this latter hypothesis (Josephy 1923;Vogt 1952;Winkelman and Book 1949), others insisted that the findings that had been reported were nonspecific in nature (Bamford and Bean 1932;Dunlap 1924;Spielmeyer 1930). More recent appraisals of these studies have concluded that all of these earlier investigations contained significant methodologicial flaws (Benes 1988).…”

Section: The Problem and The Datamentioning

confidence: 99%