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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Akinesia (or absence of movement) is a prominent feature of Parkinson's disease. Akinetic symptoms, however, are also observed in depression and schizophrenia, which support the hypothesis that akinesia involves more than only motor behavior. A common feature of these disorders is the disruption of dopamine homeostasis in the CNS. Here we aimed at relating the respective involvement of the nigrostriatal and mesocortical dopaminergic pathways to akinesia. We investigated in the rat the relative effects of selective bilateral partial lesions of substantia nigra pars compacta (SNc) or ventral tegmental area (VTA) which did not affect locomotion, on fine motor, motivational and cognitive behaviors. Motor impairments were measured by the evaluation of fine motor control in the stepping test and in the paw reaching test. Cognitive functions were assessed by various paradigms: spontaneous alternation in the Y maze and object exploration task. Motivational behavior was evaluated by the 100-pellets test. The results suggested that specific behavioral impairments are obtained following selective lesions of either SNc or VTA. SNc-lesioned rats exhibited deficits in fine motor functions as previously described in animal models of Parkinson's disease, whereas VTA-lesioned rats demonstrated traits of perseveration without significant motor impairments.
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PMID:Differential behavioral effects of partial bilateral lesions of ventral tegmental area or substantia nigra pars compacta in rats. 1845 18

Stereotaxic pallidotomy for Parkinson's disease (PD) is an old concept, which was gradually and mostly replaced by thalamotomy. Recently, posteroventral pallidotomy (PVP), originally proposed by Leksell et al., was reintroduced; this paper examines PVP in terms of its historical background, technical aspect and location of the surgical lesion, as well as clinical effects on motor and psychological symptoms. Posteroventral pallidotomy has been shown to be satisfactory in relieving rigidity and secondary akinesia, but not powerful enough in alleviating severe tremor. These are similar observations to those made in classical pallidotomy. For this reason, all PVP-treated cases reported in this paper have an additional small thalamic lesion for control of tremor. Also, it must be recognized that most of the surgically treated patients are continuing to take medication at the same or slightly lowered dose compared with preoperatively. Dopa-induced dyskinesia is alleviated well by PVP, similar to thalamotomy. The most important question is whether PVP has more effect on truncal symptoms, such as postural imbalance, and on gait than thalamotomy, a question that is still not satisfactorily answered in both clinical and basic analysis. Parkinson's disease-induced changes in emotional status, such as depression or hypochondriacal complaints, are favorably influenced by PVP, but not by thalamotomy. The role of stereotaxic surgery in the era of pharmacological treatment is discussed, as is the possible importance of the role of the limbic-motor circuit in research on PD.
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PMID:Posteroventral pallidotomy: its effect on motor symptoms and scores of MMPI test in patients with Parkinson's disease. 1859 Oct 49

Many studies have shown that early life stress may lead to impaired brain development, and may be a risk factor for developing psychiatric pathologies such as depression. However, few studies have investigated the impact that early life stress might have on the onset and development of neurodegenerative disorders, such as Parkinson's disease, which is characterized in part by the degeneration of dopaminergic neurons in the nigrostriatal pathway. The present study subjected rat pups to a maternal separation paradigm that has been shown to model adverse early life events, and investigated the effects that it has on motor deficits induced by a unilateral, intrastriatal injection of 6-hydroxydopamine (12 microg/4 microl). The female rats were assessed for behavioral changes at 28 days post-lesion with a battery of tests that are sensitive to the degree of dopamine loss. The results showed that rats that had been subjected to maternal separation display significantly impaired performance in the vibrissae and single-limb akinesia test when compared to normally reared animals. In addition, there was a significant increase in the loss of tyrosine hydroxylase staining in maternally separated rats. Our results therefore suggest that adverse experiences sustained during early life contribute to making dopamine neurons more susceptible to subsequent insults occurring during more mature stages of life and may therefore play a role in the etiopathogenesis of Parkinson's disease.
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PMID:Maternal separation exaggerates the toxic effects of 6-hydroxydopamine in rats: implications for neurodegenerative disorders. 1860 96

We describe a case of a 56 year old man with myopericarditis complicated with cardiogenic shock within first 3 days, mimicking on admission acute myocardial infarction with ST elevation in inferior ECG leads. Additionally, patient presented hyperthyroidism and totally decompensated diabetes mellitus. He required during the first 3 days intravenous infusion of inotropic agents. Cardiac enzymes levels were elevated. Akinesia in mid-inferior and mid-posterior regions in ECHO was observed. On the 10th day ST segment elevation in I, II, V3-V6 and ST depression in aVR was observed in ECG. After stabilisation patient underwent coronarography which showed normal coronary arteries. The final diagnosis was acute myopericarditis complicated with acute heart failure and cardiogenic shock.
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PMID:[Myopericarditis complicated with cardiogenic shock mimicking acute coronary syndrome with ST elevation in a patient with hyperthyroidism and diabetes mellitus]. 1892 29

We report the case of a 60-year-old woman admitted to our hospital for typical chest pain with only mild ST segment depression in the anterior precordial leads but with left ventricular akinesia of the mid-infero-postero-lateral segments with sparing of the base and of the apical septum. Coronary angiography was normal and the patient was dismissed from our hospital after echocardiographic normalization in spite of persistent ECG repolarization changes. We conclude that echocardiographic examination allows recognition of atypical forms of "tako-tsubo" disease in presence of only subtle and non-specific repolarization changes.
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PMID:Tako-tsubo syndrome: report of a case with mild electrocardiographic changes but with multiple wall motion abnormalities. 1923 Sep 92

A dopaminergic deficiency in patients with Parkinson's disease (PD) causes abnormalities of movement, behaviour, learning, and emotions. The main motor features (ie, tremor, rigidity, and akinesia) are associated with a deficiency of dopamine in the posterior putamen and the motor circuit. Hypokinesia and bradykinesia might have a dual anatomo-functional basis: hypokinesia mediated by brainstem mechanisms and bradykinesia by cortical mechanisms. The classic pathophysiological model for PD (ie, hyperactivity in the globus pallidus pars interna and substantia nigra pars reticulata) does not explain rigidity and tremor, which might be caused by changes in primary motor cortex activity. Executive functions (ie, planning and problem solving) are also impaired in early PD, but are usually not clinically noticed. These impairments are associated with dopamine deficiency in the caudate nucleus and with dysfunction of the associative and other non-motor circuits. Apathy, anxiety, and depression are the main psychiatric manifestations in untreated PD, which might be caused by ventral striatum dopaminergic deficit and depletion of serotonin and norepinephrine. In this Review we discuss the motor, cognitive, and psychiatric manifestations associated with the dopaminergic deficiency in the early phase of the parkinsonian state and the different circuits implicated, and we propose distinct mechanisms to explain the wide clinical range of PD symptoms at the time of diagnosis.
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PMID:Initial clinical manifestations of Parkinson's disease: features and pathophysiological mechanisms. 1990 11

Sleep disturbances are very common in patients with PD and are associated with a variety of negative outcomes. The evaluation of sleep disturbances in these patients is complex, as sleep may be affected by a host of primary sleep disorders, other primary medical or psychiatric conditions, reactions to medications, aging or the neuropathophysiology of PD itself. In this article, we review the evaluation of the common disturbances of sleep seen in PD. This includes the primary sleep disorders, the interaction of depression and insomnia, the impact that medications for PD have on sleep, as well as the role of factors such as nocturia, pain, dystonia, akinesia, difficulty turning in bed, and vivid dreaming. The treatment of sleep disturbances in PD is largely unstudied but recommendations based on clinical experience in PD and research studies in other geriatric populations can be made. Important principles include, diagnosis, treating the specific sleep disorder or co-occurring disorder, and control of the motor aspects of PD.
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PMID:Sleep disturbances in Parkinson's disease. 2018 36

Huntington's disease (HD) is caused by a CAG repeat expansion in exon 1 of the HD gene resulting in a long polyglutamine tract in the N-terminus of the protein huntingtin. Patients carrying the mutation display chorea in early stages followed by akinesia and sometimes dystonia in late stages. Other major symptoms include depression, anxiety, irritability or aggressive behavior, and apathy. Although many neuronal systems are affected, dysfunction and subsequent neurodegeneration in the basal ganglia and cortex are the most apparent pathologies. In HD, the primary hypothesis has been that there is an initial overactivity of glutamate neurotransmission that produces excitotoxicity followed by a series of complex changes that are different in the striatum and in the cortex. This review will focus on evidence for alterations in dopamine (DA)-glutamate interactions in HD, concentrating on the striatum and cortex. The most recent evidence points to decreases in DA and glutamate neurotransmission as the HD phenotype develops. However, there is some evidence for increased DA and glutamate functions that could be responsible for some of the early HD phenotype. Significant evidence indicates that glutamate and dopamine neurotransmission is affected in HD, compromising the fine balance in which DA modulates glutamate-induced excitation in the basal ganglia and cortex. Restoring the balance between glutamate and dopamine could be helpful to treat HD symptoms.
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PMID:Dopamine and glutamate in Huntington's disease: A balancing act. 2040 48

In this review, the symptoms contributing to the opioid-induced 'catatonia' are presented in detail, and efforts are made to relate these symptoms to opioid-induced alterations in neurotransmitter metabolism in several parts of brain, in particular in the basal ganglia. One important symptom is the muscular rigidity, which is, at least to a great part, mediated by opioid receptors in the striatum. This effect is probably not due to an action on opioid receptors located on endings of nigro-striatal dopaminergic neurones (localization I in Fig. 2), but on receptors located on neurones, the cell bodies of which are within the striatum (localization II) or much less likely on receptors on endings of glutamergic, cortico-striatal neurones (localization IV). Another characteristic symptom, the akinesia, can be induced by injections into the nucleus accumbens, which do not lead to any significant muscular rigidity. Accordingly, opioid-induced muscular rigidity and akinesia can be dissociated topographically, and it is shown by this observation that the opioid-induced 'catatonia' is due to an interference of at least two different signs. 'Catalepsy', on the other hand, is probably the consequence of a very pronounced akinesia, and spontaneously occurring rigidity does not seem to contribute to it. In addition, opioids can induce-after low doses immediately, after high doses subsequently to the depressory phase-signs of behavioural stimulation (locomotor stimulation, some stereotypic behaviour), which seem to be antagonistic to the 'catatonia' from the functional standpoint. Several types of behavioural stimulation seem to exist, with different localizations. An activation of nigro-striatal and mesolimbic dopaminergic neurones seems to be of particular relevance in the behavioural stimulation, which is due to actions of opioids on receptors located within the substantia nigra (on endings of afferent neurones, localization III in Fig. 2) and/or within the ventral tegmentum. Part of this dopaminergic activation might be, in addition, due to actions on opioid receptors located on dopaminergic nerve endings within the striatum (localization I) or the nucleus accumbens. A hypothesis for the biphasic action of opioids (first behavioural depression, then activation is presented, involving a lower sensitivity (eg affinity) of those receptors mediating 'catatonia'. Finally, it is discussed that a detailed study of opioid action on basal ganglia might perhaps give relevant information about some pathophysiological mechanisms in schizophrenic diseases, in Parkinson's disease and in psychic dependence on opioids.
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PMID:Neurochemical aspects of the opioid-induced 'catatonia'. 2048 69

Behavioral and neurochemical effects of chronic administration of high doses of 2-phenylethylamine (PEA; 25-75 mg/kg, i.p. for up to 7 days) have been investigated in Balb/c mice. Depression and anxiety, as demonstrated respectively by increased floating time in forced swim test, and reduction in number of entries and the time spent in the open arms in an elevated plus maze were observed in these animals. General motor disabilities in terms of akinesia, catalepsy and decreased swimming ability were also observed in these animals. Acute and sub-acute administration of PEA caused significant, dose-dependent depletion of striatal dopamine, and its metabolites levels. PEA caused dose-dependent generation of hydroxyl radicals in vitro in Fenton's reaction in test tubes, in isolated mitochondrial fraction, and in vivo in the striatum of mice. A significant inhibition of NADH-ubiquinone oxidoreductase (complex-I; EC: 1.6.5.3) activity suggests the inhibition in oxidative phosphorylation in the mitochondria resulting in hydroxyl radical generation. Nissl staining and TH immnunohistochemistry in brain sections failed to show any morphological aberrations in dopaminergic neurons or nerve terminals. Long-term over-consumption of PEA containing food items could be a neurological risk factor having significant pathological relevance to disease conditions such as depression or motor dysfunction. However, per-oral administration of higher doses of PEA (75-125 mg/kg; 7 days) failed to cause such overt neurochemical effects in rats, which suggested safe consumption of food items rich in this trace amine by normal population.
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PMID:2-Phenylethylamine, a constituent of chocolate and wine, causes mitochondrial complex-I inhibition, generation of hydroxyl radicals and depletion of striatal biogenic amines leading to psycho-motor dysfunctions in Balb/c mice. 2069 Dec 35


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