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Query: UMLS:C0085632 (apathy)
 4,089 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three different syndromes produced by congeners of morphine have been identified in the nondependent chronic spinal dog. These syndromes have been attributed to interaction of agonists with three distinguishable receptors (mu, kappa and sigma). Morphine is the prototype agonist for the mu receptor, ketocyclazocine for the kappa receptor and SKF-10,047 for the sigma receptor. The morphine syndrome (mu) in the dog is characterized by miosis, bradycardia, hypothermia, a general depression of the nociceptive responses and indifference to environmental stimuli. Ketocyclazocine (kappa) constricts pupils, depresses the flexor reflex and produces sedation but does not markedly alter pulse rate or the skin twitch reflex. SKF-10,047 (sigma), in contrast to morphine and ketocyclazocine, causes mydriasis, tachypnea, tachycardia and mania. The effects of these three drugs can be antagonized by the pure antagonist naltrexone, indicating that they are agonists. Further, chronic administration of morphine, ketocyclazocine and SKF-10,047 induces tolerance to their agonistic effects. Morphine suppresses abstinence in morphine-dependent dogs while ketocyclazocine does not. Ketocyclazocine at best precipitated only a liminal abstinence syndrome in the morphine-dependent dog, indicating that it had little affinity for the morphine receptor. Ketocyclazocine thus appears to be a selective agonist at the kappa receptor. Further, it has been shown that buprenorphine is a partial agonist of the mu type which both suppressed and precipitated abstinence in the morphine-dependent dog while morphine and propoxyphene are stronger agonists. Apomorphine and SKF-10,047 produce similar pharmacologic effects suggesting that sigma activity may involve a dopaminergic mechanism.
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PMID:The effects of morphine- and nalorphine- like drugs in the nondependent and morphine-dependent chronic spinal dog. 94 47

1. Normal pressure hydrocephalus (NPH) is a rare but potentially treatable form of dementia. Shunting will improve functioning in 40% to 50% of patients. 2. The classic symptoms of NPH are dementia characterized by mild memory impairment and apathy, ataxic gait, and urinary hesitancy or incontinence. 3. The patient with NPH may present with psychiatric symptoms of depression, paranoia, visual hallucinations, irrational hostility, and aggression or mania. 4. Patients with NPH are indifferent about activities of daily living and personal safety and require close supervision.
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PMID:Normal pressure hydrocephalus. A potentially reversible form of dementia. 161 84

The intercorrelations of five different factor-analytically derived syndrome solutions of the AMP-system were computed. The syndromes were based on the psychopathological symptoms of 2,269 patients on admission to the psychiatric clinic of the Free University of Berlin. The syndromes which were similar in content in the solutions of different clinics could be shown to intercorrelate quite highly. Only the different syndromes of stupor and obsession-compulsion did not show the same high degree of similarity. Between the syndromes of the solution of one clinic as well as between the solutions of different clinics high intercorrelations were computed comparing non-corresponding syndromes; this could be demonstrated for the syndromes of mania with hostility and of apathy with stupor and depression. For building syndromes in the AMDP-system in the near future the aim for independence of the syndromatic scales seems to be important.
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PMID:[A statistical comparison of the different factor analyses of the AMP-system (author's transl)]. 708 61

This study investigated emotional change following stroke at acute (2-week), 2-month, and 6-month time intervals. Five dimensions of emotional functioning were examined in a sample of 19 stroke subjects: indifference, inappropriateness, depression, mania, and pragnosia (a defect in the pragmatics of social communicative style). Results showed that, at the 2-month point, differential recovery rates become apparent depending on hemispheric side of the stroke lesion. Increased indifference, inappropriateness, and depression appear to account for these results and suggest a slower rate of recovery on these variables in the left hemisphere group (LH n = 9) compared to the right (RH n = 10). Results further indicate that, at the 6-month point, emotional functioning in RH subjects appears to worsen. In contrast, emotional recovery in LH subjects seems to stabilize at this time. Clinical implications of these findings in terms of type and timing of intervention are discussed.
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PMID:Emotional sequelae of stroke: a longitudinal perspective. 783 3

Five parallel anatomic circuits link regions of the frontal cortex to the striatum, globus pallidus/substantia nigra, and thalamus. The circuits originate in the supplementary motor area, frontal eye fields, dorsolateral prefrontal region, lateral orbito-frontal area, and anterior cingulate cortex. Open loop structures that provide input to or receive output from specific circuits share functions, cytoarchitectural features, and phylogenetic histories with the relevant circuits. The circuits mediate motor and oculomotor function as well as executive functions, socially responsive behavior, and motivation. Neuropsychiatric disorders of frontal-subcortical circuits include impaired executive function, disinhibition, and apathy; indicative mood disorders include depression, mania, and lability. Transmitters, modulators, receptor subtypes, and second messengers within the circuits provide a chemoarchitecture that can inform pharmacotherapy.
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PMID:Frontal-subcortical circuits and neuropsychiatric disorders. 750 69

We described an autopsy case of 79-year-old woman with clinically unclassified senile dementia. The patient developed forgetfulness at the age of 73, and later, persecution mania, apathy and episodic stupor, but no extrapyramidal symptoms. Neuropathological examination revealed severe neuronal loss and gliosis of substantia nigra, moderate neuronal loss and marked grumose degeneration of dentate nucleus, and mild astrocytosis of subthalamic nucleus. Abundant neurofibrillary tangles (NFT) were observed in subthalamic nucleus, globus pallidus, substantia nigra, locus ceruleus, tegmentum of brain stem, pontine nucleus, inferior olive, and dentate nucleus. Gallyas silver impregnation method showed a wide distribution of argyrophilic grains and threads in cerebrum, brain stem and cerebellum. Although absence of clinical and neuropathological hallmarks excluded the diagnosis of progressive supranuclear palsy (PSP), the distribution of NFT and argyrophilic grains in this patient resembled PSP.
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PMID:[Adult-onset dementia with abundant neurofibrillary tangles resembling progressive supranuclear palsy]. 795 13

Frontal-subcortical circuits provide a comprehensive framework for understanding the anatomy, biochemistry, and pharmacology of behavior. The three principal behaviorally relevant circuits originate in the dorsolateral prefrontal cortex, orbitofrontal cortex, and anterior cingulate cortex, respectively. Circuit-specific marker behaviors associated with each circuit are executive dysfunction (dorsolateral prefrontal-subcortical circuit), disinhibition and OCD (orbitofrontal-subcortical circuit), and apathy (medial frontal-subcortical circuit). Environmental dependency is common to all prefrontal-subcortical syndromes and may reflect disruption of working memory. Depression, mania, and psychosis are mediated by structures involved in prefrontal-subcortical circuits and are circuit-related but not circuit-specific behaviors. The actions of PCP, LSD, serotonergic antidepressants, anxiolytics, sedative-hypnotics, antipsychotic agents, and ethanol may all be partially or primarily mediated through transmitter systems and receptor effects expressed through frontal-subcortical circuits.
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PMID:Anatomic and behavioral aspects of frontal-subcortical circuits. 859 19

Numerous emotional and behavioral disorders occur following cerebrovascular lesions. Depression is the most common of these, affecting up to 40% of patients. Clinical correlates of post-stroke depression include severity of physical and cognitive impairment as well as location of brain injury. Perhaps the most compelling reason to identify post-stroke depression, however, is its substantial impact on recovery in activities of daily living, cognitive function, and survival. Antidepressant medication has been shown to effectively treat depression, although its administration may require careful clinical monitoring. Other post-stroke emotional/behavioral disorders include mania, bipolar disorder, anxiety disorder, apathy, and pathological crying. Controlled studies have not documented the effect of these disorders on long-term recovery, but the potential impact of syndromes such as mania and apathy on rehabilitation efforts or pathological crying on social functioning are evident. With the exception of pathological crying, which has been shown to respond to antidepressant drug therapy, the other post-stroke emotional/behavioral disorders need to be evaluated in controlled treatment trials for response to therapy.
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PMID:Neuropsychiatric consequences of stroke. 904 57

Numerous studies in stroke patients suggest that the left frontal anterior region may be strategic for depression. However, these findings could not always be replicated. Some authors even deny any etiological contribution of lesion location to depression. The predominant role of the right hemisphere in secondary mania is well recognized. In disorders such as apathy, anxiety, catastrophe reactions and pathological laughing and crying, further studies are needed to determine the potential clinico-topographic correlations. Affective disorders are important to consider in stroke patients, since they may influence neurological recovery and may be responsive to treatment. Remarkable features of emotional behavior, such as disinhibition, denial, indifference, overt sadness and aggressiveness, are not rare during the acute phase of stroke and might be overlooked if not searched for systematically with appropriately designed scales. Some of these early behaviors, such as denial, may relate to the late development of depression, anxiety and other disorders. Systematic studies on large samples of patients may allow to establish which of these acute emotional behavioral changes are markers for the delayed development of mood disorders.
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PMID:Affective disorders following stroke. 928 28

The frontal lobes can be subdivided into major functional neuroanatomical domains, which, when injured, surgically destroyed, or reduced in activity or volume, give rise to signature pathological and psychiatric symptomology. A review of case reports and over 50 years of research, including magnetic resonance imaging, positron emission tomography, and single photon emission computed tomography scans, indicates that apathy, "blunted" schizophrenia, major depression, and aphasic-perseverative disturbance of speech and thought are associated with left lateral as well as bilateral frontal (and striatal) abnormalities. Impulsiveness, confabulatory verbosity, grandiosity, increased sexuality, and mania are associated with right frontal (as well as bilateral) disturbances. Gegenhalten, catatonia, and disturbances of "will" are indicative of medial frontal injuries. Disinhibitory states and obsessive-compulsive perseverative abnormalities are more frequently observed with orbital frontal lobe dysfunction, including frontal-striatal disturbances. These associations, however, are not always clear-cut as patients with the same diagnosis may demonstrate different symptoms that may be due to an additional abnormality in a different region of the brain. Moreover, as the frontal subdivisions are richly interconnected, and as frontal lobe abnormalities are not always discrete or well localized, a wide array of seemingly divergent waxing and waning symptoms may be manifest, sometimes simultaneously, including manic depression and what has been referred to as the "frontal lobe personality."
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PMID:Frontal lobe psychopathology: mania, depression, confabulation, catatonia, perseveration, obsessive compulsions, and schizophrenia. 1042 Apr 28


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