Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From 1967 to 1979, 118 incident cases of idiopathic Parkinson's disease (IPD) and 236 age- and sex-matched controls from Rochester, MN, were identified. Medical records on patients and controls for 40 years preceding the diagnosis of IPD were reviewed. The relative risk (RR) for ever-smoked and IPD was not significantly different from unity (RR = 0.7, 95% confidence interval = 0.4 to 1.2). The mean age at diagnosis of IPD was significantly younger (p = 0.007) in the ever-smokers (68.8 years) compared with never-smokers (73.8 years), although this needs to be interpreted cautiously. It is concluded that smoking had no effect on the development of IPD. Within 5 years after the index date, a new diagnosis of dementia was made more often in cases than in controls (p = 0.01). Relative risk of IPD significantly increased when prior diagnosis of psychoneurosis and psychosomatic illness had been made.
 ...
PMID:A case-control study of smoking habits, dementia, and other illnesses in idiopathic Parkinson's disease. 380 3

Coined by Sifneos in 1972, alexithymia refers to a relative narrowing in emotional functioning, an inability to find appropriate words to describe their emotions, and a poverty of fantasy life. Although initially described in the context of psychosomatic illness, alexithymic characteristics may be observed in patients with a wide range of medical and psychiatric disorders: Parkinson disease, depression, anxiety, substance abuse and eating disorders. Flattening of affect and poverty of speech, major negative symptoms, referred to chronic schizophrenia: there is a lack of outward display of emotions. Accordingly, some disturbances of alexithymia's scores would be expected in schizophrenic patients. The aims of this study were: first to establish some correlations between alexithymia and some symptoms of schizophrenia, and second to estimate the intensity of alexithymia in negative versus positive and undifferentiated schizophrenic patients. Twenty-nine patients, meeting DSM III-R criteria for schizophrenia have been studied. All of them treated by neuroleptics, were in a stable clinical status for at least one month. The patients were assessed by one trained psychiatrist (IN) using six rating scales: Beth Israel Questionnaire (BIQ) for alexithymia, Positive and Negative Syndrome Scale (PANSS), Depressive Retardation Rating Scale (DRRS), Montgomery and Asberg Depression Rating Scale (MADRS), revised Physical Anhedonia Scale (PAS), and finally, Extrapyramidal Symptom Rating Scale (ESRS). In the total sample, the mean score of BIQ was 4.79 +/- 1.68 (mean +/- SD). Significant correlations were found between alexithymia and blunted affect (r = 0.376; p < 0.05), poverty of speech (r = 0.471; p < 0.01), anxiety (r = 0.370; p < 0.05), total score of DRRS (r = 0.370; p < 0.05), and motor subscore of DRRS (r = 0.429; p < 0.05). The patients with negative symptoms of schizophrenia had significantly higher total scores in alexithymia (p < 0.05), blunted affect (p < 0.0001), poverty of speech (p < 0.0001), anxiety (p < 0.05), total score of DRRS (p = 0.01) and his motor subscore (p < 0.0001) as compared to positive and undifferentiated subtypes. In our study, alexithymia seems to be correlated with negative and depressive symptoms in negative forms of schizophrenia, regardless of medication status.
 ...
PMID:[Negative symptoms, depression, anxiety and alexithymia in DSM III-R schizophrenic patients]. 941 92

Coined by Sifneos in 1972, alexithymia refers to a relative narrowing in emotional functioning, an inability to find appropriate words to describe their emotions and, a poverty of fantasy life. Although initially described in the context of psychosomatic illness, alexithymic characteristics may be observed in patients with a wide range of medical and psychiatric disorders: Parkinson disease, depression, anxiety, substance abuse and eating disorders. Flattening of affect and poverty of speech, major negative symptoms, referred to chronic schizophrenia: there is a lack of outward display of emotion. Accordingly, some disturbances of alexithymia's scores would be expected in schizophrenic patients. The purpose of this study was to estimate and compare the prevalence of alexithymia in deficit and non-deficit schizophrenia. The term "deficit symptoms" may be used as Carpenter, to refer specifically to those negative symptoms that are not considered secondary. The influence of patients' symptoms has also been studied on alexithymia scores: negative and positive symptoms of schizophrenia, depression, anxiety, anhedonia and effects of neuroleptics. Twenty-five patients, meeting DSM III-R criteria for schizophrenia have been studied. All of them treated by neuroleptics, were in a stable clinical status for at least one month. The patients have been categorized into deficit (n = 12) and non-deficit (n = 13) subgroups by one trained psychiatrist (SD), using the Schedule for the Deficit Syndrome. The subjects have been assessed by the same rater (IN), blind to deficit status, using six rating scales: Beth Israel Questionnaire (BIQ) and Toronto Alexithymia Scale (TAS) for alexithymia, Positive and Negative Syndrome Scale (PANSS), Montgomery and Asberg Depression Rating Scale (MADRS), revised Physical Anhedonia Scale (PAS), and finally, Extrapyramidal Symptom Rating Scale (ESRS). Using TAS, alexithymic characteristics were more prevalent in the deficit subgroup as compared to non-deficit subgroup (83% versus 30.76%; p < 0.01). Significant correlations were observed in the non-deficit subgroup between: TAS and anxiety (r = 0.743; p < 0.01), TAS and depression (r = 0.568; p < 0.05), BIQ and blunted affect (r = 0.636; p < 0.02), BIQ and poverty of speech (r = 0.629; p < 0.02). These correlations were not significant in the deficit group of patients. Alexithymia in schizophrenic patients seems to be a trait characteristic in deficit patients, and a state related to many symptoms, such as flattening of affect, poverty of speech, depression and anxiety in nondeficit patients.
 ...
PMID:[Alexithymia in negative symptom and non-negative symptom schizophrenia]. 945 28

The continual suppression of emotions during fight or flight reactions results in atrophy and endogenous toxicosis in noradrenergic neurons. Toxic metabolites interfere with neurotransmission, causing depression. During periodic detoxification crises, excess norepinephrine floods synapses overexcite postsynaptic neurons, and cause symptoms ranging from mild anxiety to violent behavior. When toxic metabolites, which may include excess dopamine, epinephrine, serotonin, gamma-aminobutyric acid, peptides, amino acids, and various metabolic waste products, are bound to noradrenergic receptor sites, these sites become unavailable to norepinephrine. Excitation of postsynaptic neurons is diminished and depression returns. The diverse proteins in receptor sites presumed to be specific for false neurotransmitters may instead encode specific memories. The shift in depressive and excitatory behavior is characteristic of most psychiatric disorders, addictions, Alzheimer's disease, Parkinson's disease, and psychosomatic disorders. Recovery is a detoxification process and can be facilitated by therapy that involves re-experiencing childhood traumas, releasing, and redirecting repressed emotions.
 ...
PMID:The toxic mind: the biology of mental illness and violence. 1118 26

The continual suppression of emotions during fight or flight reactions results in atrophy and endogenous toxicosis in noradrenergic neurons. Diminished synaptic levels of norepinephrine are associated with depression. During periodic detoxification crises excess norepinephrine and other metabolites flood synapses. The norepinephrine overexcites postsynaptic neurons and causes symptoms ranging from mild anxiety to violent behavior. Some of the other metabolites, which may include dopamine, epinephrine, serotonin, gamma-aminobutyric acid, peptides, amino acids, and various metabolic waste products, are bound by noradrenergic receptors and alter neurotransmission. When they prevent norepinephrine from exciting postsynaptic neurons, depression returns. A mechanism is proposed for the binding of norepinephrine and for the effects of the other metabolites, many of which have been thought to be neurotransmitters. The diverse receptor proteins presumed to be specific for false neurotransmitters may instead encode specific memories. The shift in depressive and excitatory behavior is characteristic of nearly all nervous and mental disorders, including addictions, Alzheimer's disease, Parkinson's disease, and psychosomatic disorders. When toxins accumulate in regions of the brain that control specific activities, the symptoms observed will be related to those activities, giving rise to supposedly distinct disorders that represent the same detoxification process. Recovery can be facilitated by therapy and self-help measures that involve the releasing and redirecting of repressed emotions. Full text: http://homepages.nyu.edu/~er26/toxicmind.html [corrected].
 ...
PMID:The toxic mind: the biology of mental illness and violence. 1079 Jul 41

MacLean's pioneering concept of "The Triune Brain" began to emerge in 1949 with his publication Psychosomatic disease and the "visceral brain", followed in 1952 by Some psychiatric implications of physiological studies on frontotemporal portion of limbic system (visceral brain). This shows that his seminal ideas grew out of his astute observation of psychiatric signs and symptoms. Later on, he observed the broad spectrum of human epileptic seizures and its cause in the limbic system. A large variety of uncontrolled feelings and emotions, together with bizarre motor behavior, is elicited by seizures in the hippocampus and other limbic structures.Meanwhile, based on the triune brain model, a new approach to psychopathology has taken shape. It is the evolutionary perspective of mental diseases such as the major psychoses, anorexia nervosa, anxiety disorders, and also brain diseases such as Parkinson's disease or Huntington's disease. Many mental illnesses are marked by severe deficits in social behavior and social communication. The social communication system disintegrates, especially in the major psychoses. The response choices to social or other external signals in a given situation become limited or even distorted, and reasoning is no longer part of decision making. The emphasis of this contribution is on the disintegration of social behavior in psychopathology, based on evolutionary psychiatry. MacLean's concept provides valuable insight for understanding the biological roots of human social behavior and communication. It is time to uncover the ties between the natural and the social sciences.
 ...
PMID:The place of the Triune Brain in psychiatry. 1295 43

Insidious onset of mild, unspecific, sensitive, vegetative, psychopathological, cognitive and perceptive disturbances, i.e. visual and olfactory dysfunction, with a resulting change of personal behaviour, i.e. reduced stress tolerance, precede the initially intermittently occurring motor symptoms in patients with Parkinson's disease (PD). Novel neuropathological findings suggest an expansion pattern of the neurodegenerative process beyond the nigral dopaminergic neurons with the initial event located outside the brain. We related these clinical observations of premotor symptoms of PD to this novel neuropathological concept of emerging neurodegeneration, which starts in the enteric system and then rises via spinal cord and brainstem to nigral and subsequent cortical neurons. We describe an initial premotor phase, which starts in non dopaminergic areas, and subdivide it according to the onset of gastrointestinal and brainstem associated and sensory deficits. Then motor symptoms occur and increase in the further course of PD similar to the Hoehn and Yahr stages. Our proposed diagnostic concept aims to an earlier diagnosis of PD. In addition, attention should be given to diseases of the gastrointestinal tract and psychosomatic disorders, all of which, if not or ineffectively treated, may contribute to an enhanced vulnerability for PD. The concept takes into account, that an as far unknown pathogen, e.g. viral infection or nutritional component, that meets a genetically predisposed person with a long lasting disturbed enteric nervous system, may be at risk for PD. Earlier premotor diagnosis of PD will enable more convincing future results on the therapeutic efficacy of neuroprotective compounds.
 ...
PMID:Diagnostic staging of Parkinson's disease: conceptual aspects. 1476 23