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

Growing evidence indicates that spreading depression (SD) may not only relate to some diseases, including cerebral ischemia, migraine, epilepsy, traumatic brain injury and so on, but also affect the physiological courses such as sleep patterns and general arousal. In this paper we review the relationship between SD and cerebral ischemia. The following questions are discussed: (1) The discovery of SD and its brief research history; (2) SD in the intact brain; (3) Peri-infarct SD in focal cerebral infarction. It is suggested that peri-infarct SD contributes to the growth of focal ischemic lesions, and the suppression of SD may become a novel, even a key therapeutic approach for minimizing infarct volume and protecting ischemic neurons after focal cerebral ischemia.
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PMID:[Spreading depression and cerebral ischemia]. 1253 23

Recent studies have shown that the complication rate of silent cerebral infarction (SCI) in patients with geriatric depression increases with the age at the onset of depression. This study investigated the cardiovascular factors involved in the development of SCI in geriatric depression. Thirty-six patients with geriatric depression were classified according to the age at onset into 16 who developed depression at the age of <50 years (early-onset group) and 20 who developed depression at the age of > or =50 years (late-onset group). The incidence of SCI assessed by subcortical hyperintensity on MRI images, office blood pressure (BP), nocturnal systolic BP fall pattern examined by 24-hour ambulatory BP monitoring, and the severity of carotid atherosclerosis examined by B-mode ultrasonography were compared between the two groups. Furthermore, the association between the presence or absence of SCI and the nocturnal systolic BP fall pattern or the severity of carotid atherosclerosis was evaluated. The SCI complication rate was higher in the late-onset group (55.0%) than in the early-onset group (18.7%). The office BP and mean 24-hour BP did not differ significantly between the two groups. Abnormal nocturnal systolic BP fall patterns were observed in 85.0% (nondipper type showing a fall of <10% in 60.0%, extreme-dipper type showing a fall of > or =20% in 25.0%) in the late-onset group, which was significantly higher than the incidence in the early-onset group (18.7%). No significant difference was observed in any parameter of carotid atherosclerosis between the two groups. In addition, the patients with SCI more frequently showed abnormal nocturnal systolic BP fall patterns than those without SCI. These results suggest that abnormal nocturnal BP fall patterns appear to be involved in the development of SCI in senile-onset depression.
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PMID:Abnormal nocturnal blood pressure fall in senile-onset depression with subcortical silent cerebral infarction. 1282 41

Bruxism characterized by clenching and grinding of teeth can lead to toothwear, headaches and depression. While bruxism has been associated with a number of neurological diseases, it has not been highlighted following cerebral infarction. An elderly man presented with an acute onset of tooth grinding and jaw clenching associated with dysarthria. His bruxism was worse during the day and resolved during sleep. He had frequent jaw aches, headaches and swallowing difficulty. Examination demonstrated the presence of dysarthria with jaw clenching and tooth grinding, producing persistent high pitch and loud squeaky sounds. A magnetic resonance imaging and angiography examination revealed a recent infarct in the right thalamus. In addition, chronic lacunar infarcts were present in the bilateral caudate nuclei with severe basilar artery stenosis. He was successfully treated with botulinum toxin. We discuss the pathophysiologic mechanisms of bruxism associated with basal ganglia infarcts. Dysfunction of the efferent and/or afferent thalamic or striatopallidal tracts may play a role in bruxism. Early recognition of bruxism following stroke could reduce unnecessary suffering since the condition can be effectively treated.
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PMID:Severe bruxism following basal ganglia infarcts: insights into pathophysiology. 1470 29

The mortality of stroke is still the those of single organs. Even if patients survive the brain attack they often suffer from not only motor functional disability but also psychiatric problems such as post-stroke depression and decrease in spontaneity. The stoke is the number one cause of the bed-ridden state "Netakiri". Presently only anti-thrombotic and anti-oxidative stress therapies are available and the ischemic core destroyed immediately after the stroke could never be rescued. We have started to study the basic aspect of transplantation therapy of cerebral infarction using neural stem cells. Using a focal ischemic model of the gerbil by repeated occlusion of the unilateral carotid artery, we grafted human neural stem cells which were cultured and proliferated for a long period. Grafted animals showed significant and marked improvement in all three functions including motor, sensory and cognitive functions associated with a significant reduction of infarction volume. Synaptic contacts between neurons from grafted human neural stem cells and host neurons were confirmed by immuno-electron microscopy. This is a very encouraging report although it is necessary to elucidate the precise mechanism of the functional recovery or the effect of neural stem cell transplantation.
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PMID:[Brain ischemia--regenerative therapy using human neural stem cells]. 1515 78

Four term babies, three boys and one girl, became cyanotic shortly after birth. In two cases the cause was maternal use of drugs: methemoglobinaemia due to use of a chromate and depression of the nervous system due to clomipramine. They recovered. A third child suffered cerebral infarction and was left with decreased left-arm function. The fourth child had a hypoplastic left heart and died. Central cyanosis in a newborn should be cause for concern. A thorough case history should be taken and extensive physical examination carried out. In case of doubt additional diagnostic tests should be performed.
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PMID:[Non-respiratory cyanosis in the newborn]. 1545 24

At 1997, Alexopoulos and Krishnan coined the term "vascular depression" to describe depression associated with cerebrovascular disease. Vascular depression included both post-stroke depression, depression occurring after a stroke, and MRI-defined vascular depression in which cerebral infarction is detected by magnetic resonance imaging findings. Post-stroke depression is well known as showing cerebral infarction on imaging modalities as well as clinical symptoms such as localized neurological symptoms related to infarcts. MRI-defined vascular depression demonstrates cerebral infarction on imaging modalities, but there are no clinical symptoms such as localized neurological symptoms or stroke. MRI-defined vascular depression is equivalent to the term "depression with silent cerebral infarction", a condition we studied in the past decade. When the accumulation of infarct lesions induces obstruction in the neuron network related to mood and will exceeds a certain threshold, the patient becomes predisposed to vascular depression. Neurological factors are more prominent than genetic factors or psychosocial stressors in patients with vascular depression due to an accumulation of infarct lesions. Anti-cholinergic drugs and anti-dopaminergic drugs easily induce adverse central nervous system reactions in patients with vascular depression demonstrating prominent neurological factors. Research on vascular depression has contributed to clarifying the onset mechanism of endogenous depression.
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PMID:[Asymptomatic cerebral infarction and depression--the concept of vascular depression]. 1517 94

Carotid artery dissection followed by cerebral infarction as a result of blunt trauma can occur in a number of forensically relevant situations. We describe two such cases. In the first case, a 19-year-old female was involved in a road traffic accident, when her car crashed into the rear of another car. Initially, the young woman presented a minor head injury without loss of consciousness and minor bruising to the left side of the neck. After 48 h, she had developed confusion, speech difficulties, right facial nerve paralysis, and right hemiplegia. CT scan and carotid angiography showed cerebral ischemia with infarction in the territory of the middle left cerebral artery and complete dissection of the left carotid artery. In the second case, a 33-year-old male with depression attempted to hang himself. The rope gave way and he fell down. He had also taken a paracetamol, and a non-steroidal anti-inflammatory drug overdose. He did not lose consciousness but appeared withdrawn and depressed. Approximately 6 h later, his conscious state deteriorated. A CT scan revealed thrombosis of the left internal carotid artery, extending to the middle cerebral artery. The patient died. Both cases reinforce the need for full neurological assessment and review of any individual subject to blunt trauma to the neck, whether accidental or deliberate or where the history is incomplete. In the forensic setting, in particular, RTAs, suspension by the neck, strangulation, and garotting are all instances when examination and assessment must be thorough--and clear advice given--in the absence of any immediate signs or symptoms--that any new symptoms or signs require immediate and thorough neurological investigation. There should be low threshold for prolonged neurological observation or further neurovascular investigations such as ultrasound, CT or MRI scan or angiography, to minimize the risk of developing potentially fatal or incapacitating sequelae.
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PMID:Delayed presentation of carotid dissection, cerebral ischemia, and infarction following blunt trauma: two cases. 1527 48

Preconditioning the rat brain with spreading depression for 48 h induces potent ischemic tolerance (infarct tolerance) after an interval of 12-15 days, consequently reducing the infarcted lesion size in the acute phase following focal cerebral ischemia. However, persistence of the morphological and functional neuroprotection has not yet been proven. We tested whether tolerance-derived neuroprotection against focal cerebral ischemia persists or merely delays the progress of cerebral infarction. Prolonged spreading depression was induced in mice by placing a depolarized focus with intracerebral microinfusion of KCl for 24 h; after intervals of 3, 6, 9 or 12 days, temporary focal ischemia was imposed. In the analysis of the infarcted lesion volume 24 h after ischemia, groups with 6 or 9 day interval demonstrated significantly smaller lesion volume compared to time-matched vehicle control group (P=0.002). Significant reduction in cerebral infarction was also observed at the chronic phase, namely 14 days after ischemia (33% reduction) (P=0.021) accompanied with less severe neurological deficits (38% reduction) (P=0.020). Using this technique, we also investigated if the mice with targeted disruption of a single BDNF allele (heterozygous BDNF-deficient mice) can gain the same potency of tolerance as the wild mice. In the result on infarcted lesion volumes following temporary focal ischemia, potent tolerance developed in the wild type (35% reduction) (P=0.007) but not in the heterozygous BDNF-deficient mice (<19% reduction) (P=0.155), indicating that BDNF expression level following spreading depression is contributing to infarct tolerance development.
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PMID:Spreading depression induces long-lasting brain protection against infarcted lesion development via BDNF gene-dependent mechanism. 1530 52

A 55-year-old man was admitted to our hospital because of somnolence and aspontaneity. He was hospitalized in the psychopathic ward under the initial diagnosis of depression. Chest X-ray showed infiltration in both upper lobe. Twelve days later, Mycobacterium tuberculosis was detected from his sputum and was confirmed by RT-PCR. Cerebrospinal fluid findings showed elevated ADA and mononuclear cells, suggesting the presence of tuberculous meningitis. However, the brain CT revealed no abnormal findings. By applying antituberculous treatment the pulmonary lesion improved but psychological symptoms remained. Three months later follow-up brain MRI was examined. Contrast enhanced granuloma was detected in the ambiens, suprasellar and quadrigeminal cisterns. A strong signal was seen in the left frontal thalamus and a weak enhanced lesion was detected in the right frontal thalamus on a T2 enhanced image. These lesions showed low intensity on a T1 enhanced image, suggesting cerebral infarction affecting the bilateral thalamus. Somnolence and memory disorder was due to cerebral infarction of the bilateral thalamus and tuberculous meningitis contributed to form the intracranial lesion. From the experience of this case, it is needed to consider cerebral infarction (especially the thalamus) due to tuberculous meningitis when we examine the patients with acute onset of psychological symptoms.
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PMID:[Acute onset of somnolence and amnesia due to cerebral infarction of bilateral thalamus accompanied with tuberculous meningitis: a case report]. 1548 30

We sought to evaluate the prevalence of and risk factors for post-stroke depression (PSD) at long-term follow-up in young adults aged 15-49 years with first-ever cerebral infarction in a population-based study. Scores on Montgomery-Asberg Depression Rating Scale (MADRS) were obtained at follow-up (mean time 6.0 years after the stroke) and analysed in subgroups. MADRS scores were obtained in 196 of 209 surviving patients. PSD (MADRS>or=7) was detected in 56 patients (28.6%). None had severe PSD. Alcoholism (P=0.006), depressive symptoms any time before the index stroke (P=0.016), and severe neurological deficits on admission for the index stroke (P=0.043) were independently associated with PSD. PSD seems milder in young ischaemic stroke patients compared with older patients. Alcoholism, depression any time before the index stroke, and severity of neurological deficits on admission for the stroke increased the risk of developing PSD in the long run.
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PMID:Mild depression in young adults with cerebral infarction at long-term follow-up: a population-based study. 1569 8


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