Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with factitious illness present a particular challenge. Because they may be clever in their deception, they may be difficult to recognize as the fabricators of their apparent medical problem(s). Findings vary from relatively simple problems such as fever to more complex and often dramatic complaints of bleeding and pain. Differential diagnosis should include other, often more easily managed disorders such as somatoform disorders, malingering, antisocial personality, and schizophrenia. Because no definitive treatment exists, patients often consult many physicians, often in diverse geographical locations.
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PMID:Factitious illness. Dramatic deceit versus reality. 663 26

To characterize violent behavior in hospitalized medical and surgical patients, we reviewed documented violent incidents at the San Francisco General Hospital during a two-year period. Twenty-nine incidents of verbal and physical violence occurred. One patient was gravely ill and three were delirious. All the incidents were associated with increased levels of tension and loss of impulse control. In most cases, contention with the staff regarding pain medication or ward regulations was a precipitating event. Of the 28 patients with mental disorders, 19 were substance abusers, six had organic brain syndrome, tw had neurosis, and one had schizophrenia. The findings suggest that physicians should be more sensitive to patient characteristics and to the situational characteristics of the violent incident. Explicit measures that anticipate and reduce violent behavior are reviewed.
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PMID:Violent Behavior among hospitalized medical and surgical patients. 705 53

Under examination there were 60 patients with slowly progressing hypochondriacal schizophrenia. Two variants of the disease differing in both the manifestations, form and progress rate were specified. Regularities of the time course of the psychopathological disorders classed with these variants were disclosed. In the first variant the local senestalgias were followed by a stable "neurotic-hypochondriacal" pain syndrome and terminated in formation of superdominant hypochondria. In the second variant the clinical picture of the disease that starts from diffuse, migrating senestalgias later expands due to addition of senesthetic and hystero-conversive disorders and terminated in formation of the syndrome of obsessive hypochondria.
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PMID:[Onset of slowly progressive hypochondriacal schizophrenia]. 706 13

Ten patients with the stable syndrome of hysteria were matched for age, sex, handedness, and full-scale WAIS IQ with ten controls, ten psychotic depressives and ten schizophrenics. All were subjected to an extensive neuropsychological test battery. Compared to the controls, the hysteria group exhibited bifrontal impairment (R = L) and, globally, greater dysfunction of the nondominant hemisphere. A G analysis provided a complete separation between the hysteria and controls. However, a D-index analysis showed that the hysteria group was more impaired than normals and depressives because of greater dysfunction of the dominant hemisphere, whilst schizophrenia showed greater nondominant hemisphere dysfunction than hysteria. Further, a cluster analysis on the 40 subjects produced three clusters: normal controls, depressives, and a schizophrenia-hysteria grouping. These findings are interpreted as suggesting that dominant hemisphere dysfunction is fundamentally related to the syndrome of hysteria and that the dysfunction of the nondominant hemisphere is brought about by associated features: the female excess, the emotional instability and dysphoric mood, the presence of asymmetrical pain, and conversion symptomatology. It is further argued, in view of the familial associations, that hysteria in the female is a syndrome equivalent to psychopathy in the male (who also exhibits dominant hemisphere dysfunction) and might represent in the female a (relatively benign) variant of schizophrenia characterized by imprecise verbal communications, a subtle form of affective incongruity, together with the conversion parameter.
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PMID:A neuropsychological study of the stable syndrome of hysteria. 727 78

In an examination of the phenomenology of pain in 78 patients with schizophrenia, 29 had current pain complaints. Of these 13 had an appropriate physical cause, leaving 16 with pain of seemingly psychological origin. The head, leg and back were the commonest sites. Complaints were most often described in sensory terms. Pain plausibly related to a specific delusion or hallucinatory process occurred only once, and no gross examples of insensitivity to noxious stimuli or to self-mutilation were seen. Patients with schizophrenia may have less pain than those with anxiety or depression but certainly do experience pain both from physical and psychological causes. The influence of phenothiazines on pain experience is uncertain.
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PMID:Relationships between pain and schizophrenia. 727 36

Broen and Storms have developed a popular behavioristic theory to explain schizophrenic thought disorder. It holds that thought disorder results from schizophrenics' having higher drive levels and lower response-strength ceilings than non-schizophrenics. As a result, the strength of appropriate (usually strong) responses is rivaled by that of inappropriate, ordinarily-weak responses. This, in Broen and Storms' theory, is the cause of disorganized, schizophrenic behavior. We tested several hypotheses derived from Broen and Storms' assumptions that schizophrenics have higher drive and lower response strength ceilings than controls in a paired-associates learning study. We did not find support for our hypotheses that schizophrenics would show better early-trials learning than controls, that a presumably drive-inducing threat of pain would enhance early trials learning in schizophrenics or controls, that either threat of pain or schizophrenia would be associated with a low learning asymptote, or that either the positive or negative effects of pain would be accentuated in schizophrenics. The results did not support the theory.
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PMID:A test of the Broen-Storms theory of cognitive deficit in schizophrenia. 730 58

A qualitative study using interpretive interactionism investigated how individuals with schizophrenia develop an ability to detect early signs of relapse. A purposive sample of 15 respondents were interviewed about their illness experiences. Three sequential processes were identified. Responding reactively to psychic pain, initiated by a desire to escape from overwhelming distress, resulted in the differentiation of tolerable and intolerable pain. Refining perceptions of psychic pain followed and resulted in the identification of specific thoughts, feelings and behaviors associated with different levels of distress. Finally, actively reducing psychic pain resulted in a proactive surveillance for specific signs of increasing distress.
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PMID:The development of the self-care ability to detect early signs of relapse among individuals who have schizophrenia. 748 67

Neuropeptide Y (NPY) is a 36-amino acid peptide belonging to the pancreatic polypeptide family that has marked and diverse biological activity across species. NPY originally was isolated from mammalian brain tissue somewhat more than 10 years ago and, since that time, has been the subject of numerous scientific publications. NPY and its proposed three receptors (Y1, Y2 and Y3) are relatively abundant in and uniquely distributed throughout the brain and spinal cord. This review will highlight the results from a number of research-oriented studies that have examined how NPY is involved in CNS function and behavior, and how these studies may relate to the possible development of medicines, either NPY-like agonists or antagonists, directed towards the treatment of disorders such as anxiety, pain, hypertension, schizophrenia, memory dysfunction, abnormal eating behavior and depression.
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PMID:Central nervous system pharmacology of neuropeptide Y. 764 68

For pharmaceuticals ranging from digitalis to vincristine the ethnobotanical approach to drug discovery has proven successful. The advent of high-throughput, mechanism-based in vitro bioassays coupled with candidate plants derived from pain-staking ethnopharmacological research has resulted in the discovery of new pharmaceuticals such as prostratin, a drug candidate for treatment of human immunodeficiency virus, as well as a variety of novel antiinflammatory compounds. Not all Western diseases are equally likely to be recognized by indigenous peoples. Gastrointestinal maladies, inflammation, skin infections and certain viral diseases are likely to be of high saliency to indigenous healers, whereas diseases such as cancer and cardiovascular illness are unlikely to be easily diagnosed by indigenous peoples. Yet indigenous remedies may indicate pharmacological activity for maladies such as schizophrenia, for which the biochemical mechanisms have yet to be discovered. Ethnopharmacological information can be used to provide three levels of resolution in the search for new drugs: (1) as a general indicator of non-specific bioactivity suitable for a panel of broad screens; (2) as an indicator of specific bioactivity suitable for particular high-resolution bioassays; (3) as an indicator of pharmacological activity for which mechanism-based bioassays have yet to be developed.
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PMID:The ethnobotanical approach to drug discovery: strengths and limitations. 773 59

In this paper a detailed argument will be advanced in support of the notion that schizophrenia is fundamentally a diabetic brain state, henceforth referred to as 'cerebral diabetes'. Many extraneous features of cerebral diabetes have been observed, including positron emission tomography (PET) scans which reflect abnormal distribution patterns and diminished supplies of glucose in the brain. Equally, empirical research has demonstrated that plasma levels of essential fatty acids and prostaglandins are abnormally low, and low levels of glycoproteins in the urine of cerebral diabetics have also been observed. In addition, cerebral diabetics manifest a wide range of disturbing physical symptoms, such as, impaired sexual function, temperature control, low blood pressure, disrupted sleep patterns, excessive thirst, poor memory, insensitivity to pain, and chronic unhappiness, all of which can be attributed to disrupted neuroendocrine function. Thus, in order to persuasively assert the redefinition of schizophrenia as 'cerebral diabetes', we shall first explicate glucose regulation and transport in the brain and then outline how this interacts with essential fatty acids and prostaglandins, neurotransmission, and the neuroendocrine system. In so doing, we shall provide a metabolic explanation for all the prominent symptoms currently known to be associated with cerebral diabetes and indicate some future therapeutic interventions.
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PMID:Schizophrenia is a diabetic brain state: an elucidation of impaired neurometabolism. 773 17


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