Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some diseases develop dementia, but they may be dementia-like-situation, such as depression and drugs induced one. There are many causes as an etiology of dementia. Among them a lots of diseases are treatable dementia, like chronic subdural hematoma, normal pressure hydrocephalus, brain abscess, syphilis, herpetic encephalitis, Wilson's disease, hypothyroidism, parathyroid disease, vitamin B12 deficiency, pellagra etc. In examination of patients with dementia, exact history taking, physical examination and laboratory examination should be done carefully. In the patients with Alzheimer's dementia and cerebrovascular disease's dementia, as many risk factors are known, we must try to treat and exclude each risk factor and protect the dementia. Inactivity of physical and mental function is reported to induce the dementia, so activation of them could prevent the development and the progression of dementia. In future the methods of the prevention of apoptosis and cell death would be found in order to prevent the dementia. Free radical scavenger, nerve trophic factor, cytokine, antagonist of glutamate etc. will have the possibility to become the medicine for the dementia. The nerve transplantation, nerve transmitter, nerve peptide etc. might serve as the allopathic treatment for the dementia.
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PMID:[Aging of brain and the maintenance of the function]. 875 27

Clinical electroencephalography is a relatively simple and inexpensive diagnostic tool with a high sensitivity for diffuse organic encephalopathy of various aetiologies but with a rather low specificity for the type of diagnosis. The highest sensitivity is shown in DAT and Parkinson dementia, and in these conditions the degree of EEG abnormality is correlated with the disease severity. Quantification of EEG makes these correlations more reliable and provides a method for monitoring therapeutic effects. Dementias with predominantly frontal pathology show much less EEG abnormality, and in these conditions the EEG is often normal despite obvious clinical dementia. Also, alcohol dementias often show normal EEG patterns. At an early stage of clinical evaluation, EEG may be useful in the discrimination of organic dementia from pseudodementia, because EEG is usually normal in depression, confusion, agitation and other psychiatric conditions. In pseudodementia due to intoxication with sedatives the EEG is usually dominated by diffuse beta activity. At the stage of differential diagnosis of an organic brain disorder, EEG cannot reliably discriminate between encephalopathies secondary to hydrocephalus, AIDS, cerebrovascular disease, B12 deficiency and primary degenerative diseases such as DAT. More specific EEG patterns are seen in acute cerebrovascular lesions, metabolic encephalopathies, i.e. of hepatic origin, Creutzfeldt-Jakob disease, herpes encephalitis, and nonconvulsive status epilepticus as possible causes of a rapidly deteriorating mental and neurological condition. Repeated EEG recordings over time would add significantly to the diagnostic information. New techniques such as topographical brain mapping, analysis of the EEG during REM sleep, coherence analysis of the EEG activity, and the combination of quantified EEG techniques with evoked potentials and event-related potentials will presumably add to the sensitivity as well as the specificity of the electrophysiological methods in the diagnosis of dementia.
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PMID:Electroencephalography as a diagnostic tool in dementia. 906 24

The physicochemical properties of water enable it to act as a solvent for electrolytes, and to influence the molecular configuration and hence the function--enzymatic in particular--of polypeptide chains in biological systems. The association of water with electrolytes determines the osmotic regulation of cell volume and allows the establishment of the transmembrane ion concentration gradients that underlie nerve excitation and impulse conduction. Fluid in the central nervous system is distributed in the intracellular and extracellular spaces (ICS, ECS) of the brain parenchyma, the cerebrospinal fluid, and the vascular compartment--the brain capillaries and small arteries and veins. Regulated exchange of fluid between these various compartments occurs at the blood-brain barrier (BBB), and at the ventricular ependyma and choroid plexus, and, on the brain surface, at the pia mater. The normal BBB is relatively permeable to water, but considerably less so to ions, including the principal electrolytes Brain fluid regulation takes place within the context of systemic fluid volume control, which depends on the mutual interaction of osmo-, volume-, and pressure-receptors in the hypothalamus, heart and kidney, hormones such as vasopressin, renin-angiotensin, aldosterone, atriopeptins, and digitalis-like immunoreactive substance, and their respective sites of action. Evidence for specific transport capabilities of the cerebral capillary endothelium, for example high Na+K(+)-ATPase activity and the presence at the abluminal surface of a Na(+)--H+ antiporter, suggests that cerebral microvessels play a more active part in brain volume regulation and ion homoeostasis than do capillaries in other vascular beds. The normal brain ECS amounts to 12-19% of brain volume, and is markedly reduced in anoxia, ischaemia, metabolic poisoning, spreading depression, and conventional procedures for histological fixation. The asymmetrical distributions of Na+ K+ and Ca2+ between ICS and ECS underlie the roles of these cations in nerve excitation and conduction, and in signal transduction. The relatively large volume of the CSF, and extensive diffusional exchange of many substances between brain ECS and CSF, augment the ion-homeostasing capacity of the ECS. The choroid plexus, in addition to secreting CSF principally by biochemical mechanisms (there is an additional small component from the extracellular fluid), actively transports some substances from the blood (e.g. nucleotides and ascorbic acid), and actively removes others from the CSF. In contrast with CSF secretion, CSF reabsorption is principally a biomechanical process, passively dependent on the CSF-dural sinus pressure gradient. Pathological increases in intracranial water content imply development of an intracranial mass lesion. The additional water may be distributed diffusely within the brain parenchyma as brain oedema, as a cyst, or as increase in ventricular volume due to hydrocephalus. Brain oedema is classified on the basis of pathophysiology into four categories, vasogenic, cytotoxic, osmotic and hydrostatic. The clinical conditions in which brain oedema presents the greatest problems are tumour, ischaemia, and head injury. Peritumoural oedema is predominantly vasogenic and related to BBB dysfunction. Ischaemic oedema is initially cytotoxic, with a shift of Na+ and CI- ions from ECS to ICS, followed by osmotically obliged water, this shift can be detected by diffusion-weighted MRI. Later in the evolution of an ischaemic lesion the oedema becomes vasogenic, with disruption of the BBB. Recent imaging studies in patients with head injury suggest that the development of traumatic brain oedema may follow a biphasic time course similar to that of ischaemic oedema. Hydrocephalus is associated in the great majority of cases with an obstruction to the circulation or drainage of CSF, or, occasionally, with overproduction of CSF by a choroid plexus papilloma. In either case, the consequence is a ris
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PMID:The normal and pathological physiology of brain water. 907 71

Accurate diagnosis of dementia is essential to provide appropriate treatment as well as patient and family counseling. It may be difficult to differentiate dementia from delirium. In addition, several features distinguish dementia from depression, but the two can coexist and the distinction may be uncertain. Dementias can be grouped into two categories: dementia that presents without prominent motor signs and dementia that presents with prominent motor signs. Dementias without prominent motor signs include Alzheimer's disease, frontotemporal dementia, and Creutzfeld-Jakob and other prion diseases. Dementias characterized at onset by prominent motor signs include dementias with Lewy bodies, idiopathic Parkinson's disease, progressive supranuclear palsy, cortico-basal ganglionic degeneration, hydrocephalus, Huntington's disease, and vascular dementia. Routine diagnostic steps include a careful history, mental status screening, laboratory and imaging studies, and neuropsychologic testing. Genetic testing is available, but its use is controversial and raises complex ethical questions.
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PMID:Differential diagnosis of Alzheimer's disease. 915 54

Although the dorsal midbrain has been implicated in cognitive processes in animals, its role in humans is unclear. We report the neuropsychological and postmortem neuropathological findings of a 52-yr-old university professor who developed a profound dementia in association with a focal dorsal midbrain lesion. The patient's disorder appeared to result from a tuberculous granuloma based on the clinical course and autopsy results. Neuropsychologically, he exhibited a generalized impairment across most of the cognitive domains assessed. His deficits were not explained by impaired arousal, specific sensory or motor defects, depression, or hydrocephalus. Although there are inherent limitations to a single-case investigation, our observations are consistent with animal studies that have demonstrated that focal dorsal midbrain lesions may result in cognitive impairment. We propose that the dorsal midbrain is involved in cognitive processing via modulation of thalamocortical networks.
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PMID:Dementia associated with dorsal midbrain lesion. 937 85

A 3-month-old female Dalmatian dog and a 2.5-month-old Poodle dog were referred with a sudden onset of neurological syndrome consistent with hydrocephalus. Clinical signs included depression, severe ataxia, eye abnormalities and skull enlargement in one case. Postmortem examination revealed severe internal hydrocephalus with cavitation of the cerebral white matter associated with necrotizing and inflammatory lesions of the periventricular nervous tissue. Although no bacteria were isolated from cerebrospinal fluid and no infectious agents were detected in the brains, an infectious etiology was postulated.
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PMID:Hydrocephalus with periventricular encephalitis in the dog. 946 79

From July 1991 to June 1997. 15 neonates with Chiari type II malformation were treated at our institution. Four of them required posterior fossa decompression and cervical laminectomy for hindbrain decompression. We report anesthesia and postoperative management in these four patients. They had a fetal diagnosis of hydrocephalus and was delivered by caesarean section. They underwent Ommaya reservoir placement for drainage and repair of myelomeningocele in the neonatal period. They developed respiratory depression as apneic spells or retraction with or without swallowing difficulties and underwent posterior fossa decompression and cervical laminectomy at 20-87 days of life. One patient died of asthma at the age of 2 years and 8 days and others are doing well. Patients with this malformation may develop respiratory depression such as apneic spells and vocal cord paralysis even if the intracranial pressure is well controlled and they should be monitored carefully for the signs of apnea and the compromised airway.
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PMID:[Anesthesia and perioperative management in infants with Chiari type II malformation]. 975 65

A 58-year-old man had long-standing lesions of presumed large plaque parapsoriasis. Following treatment for nodal Hodgkin's disease (HD), these became more infiltrated, with a diagnosis of mycosis fungoides (MF). A few months later, nodules appeared on the right leg, which was lymphoedematous after inguinal irradiation for HD. Histopathological examination showed CD3+, CD30-, CD15- large pleomorphic lymphocytes, leading to the diagnosis of transformed MF. The cutaneous lesions were successfully treated with topical nitrogen mustard and interferon alfa-2b then methotrexate, but his general health worsened with depression and malaise, without specific neurological symptoms or extracutaneous spreading of the lymphoma. Cerebral computed tomographic scan revealed a cerebellar subdural collection, arachnoid cyst and quadriventricular hydrocephaly, initially considered to be non-specific. After a few weeks, clinical symptoms of intracranial hypertension appeared, and a cerebrospinal fluid (CSF) examination revealed meningeal involvement by the lymphoma. These cells were CD3-negative and the diagnosis was confirmed by polymerase chain reaction (PCR) study, which revealed an identical clonal rearrangement of the T-cell receptor gamma gene between cutaneous biopsies and the CSF. Repeated intrathecal injections of methotrexate and cranial irradiation were performed and the patient was still alive after 13 months. This case illustrates the possible meningeal involvement of MF that may be preceded by atypical and mild neurological or psychiatric symptoms, which may be dissociated from the evolution of the cutaneous lesions. Moreover, PCR study may be useful for both diagnosis and monitoring.
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PMID:Meningeal involvement by a transformed mycosis fungoides following Hodgkin's disease. 1058 78

John Cheyne (1777-1836), a Scotsman born in Leith, graduated at Edinburgh University but spent most of his career in Dublin. He was professor of medicine (1813-19) at the Royal College of Surgeons in Ireland, physician to the House of Industry Hospitals and co-founder of the Dublin Hospital Reports in which his celebrated account of a patient with irregular breathing was described in 1818. His Essay on hydrocephalus acutus (1808) and Cases of apoplexy and lethargy (1812), important nineteenth-century contributions to neuropathology are considered here in detail. Towards the end of his life he was afflicted by depression and his posthumously-published Essays on the partial derangement of the mind (1843) was written as a therapeutic exercise.
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PMID:John Cheyne's classic monographs. 1161 12

The urologic literature suggests that there is an association between a variety of psychiatric disorders and incontinence. Most notably, depression is found in a significant percentage of patients with urinary incontinence. Depression also occurs in other conditions associated with urinary urge incontinence, such as aging and dementia, and in neurologic disorders such as normal pressure hydrocephalus. Correction of some neurologic disorders eliminates both depression and urge incontinence. Although chronic medical disorders such as urge incontinence may lead to depression, an alternative hypothesis is that these two conditions share a common neurochemical pathogenesis. Lowering monoamines such as serotonin and noradrenaline in the central nervous system (CNS) leads to depression and urinary frequency and a hyperactive bladder in experimental animals. Thus, depression may not only be the result of persistent urinary incontinence, but individuals with altered CNS monoamines could manifest both depression and an overactive bladder. The latter condition may lead to urge incontinence, urinary frequency, urgency, or enuresis. Uncovering further evidence for such a linkage could serve as the basis for the development of genetic markers and novel therapeutic interventions for these two conditions.
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PMID:Depression and incontinence. 1176 Jul 84


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