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)

There is growing evidence that a variety of symptoms can precede the classical motor features of Parkinson's disease (PD). The period when these symptoms arise can be referred to as the premotor phase of the disease. Well-documented premotor symptoms in PD include constipation, loss of smell, sleep disturbances such as REM sleep behavior disorder (RBD), and mood disturbances like depression. Diagnostic and therapeutic implications linked to improved identification of these premotor features are discussed.
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PMID:The premotor phase of Parkinson's disease. 1768 39

Perillae Herba (a leaf of Perilla frutescens) has been prescribed as one of the component herbs in certain Kampo (Japanese herbal) medicines that are used clinically for the improvement of depressive mood. l-Perillaldehyde (PAH) is a major component in the essential oil containing in Perillae Herba, but its antidepressant-like effect has not been reported. To clarify the antidepressant-like effect of PAH, the inhaled effect of PAH on stress-induced depression-like model mice prepared by subjection to a combination of forced swimming and chronic mild stresses was investigated. The degree of the depression-like state was measured by the animal's duration of immobility using a forced swimming test. Inhalation of PAH (0.0965 and 0.965 mg/mouse/day, 9 days) significantly shortened the duration of immobility of the depression-like model mice and did not affect locomotor activity. However, another odor substance, cinnamaldehyde containing in Cinnamomi Cortex, exhibited no reduction in the immobility. The reduction in the immobility induced by the inhalation of PAH was prevented on anosmia-induced mice prepared by intranasal irrigation with zinc sulfate. These results suggest that the inhalation of PAH shows antidepressant-like activity through the olfactory nervous function.
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PMID:Antidepressant-like Effect of l-perillaldehyde in Stress-induced Depression-like Model Mice through Regulation of the Olfactory Nervous System. 1895 54

A solvent can be defined as "a liquid that has the ability to dissolve, suspend or extract other materials, without chemical change to the material or solvent". Numerous chemical or technical processes rely on these specific properties of organic solvents in industry. Occupational exposure to solvents is not rare and some activities may cause substantial exposure to these substances in the workforce. Short-term or acute exposures cause a prenarcotic syndrome, and long lasting exposure conditions have been associated with various neurological and neuropsychiatric disorders, e.g., anosmia, hearing loss, colour vision dysfunctions, peripheral polyneuropathy and depression, but most significantly with the gradual development of an irreversible toxic encephalopathy. For the last 3 decades reports and epidemiological studies have been published reporting sleep disturbances among other complaints, related to long-term exposure to these compounds. In addition, the question has been posed if solvents can be the cause of a sleep apnoea syndrome in exposed workers, or on the contrary, if these workers are misdiagnosed and 'common' sleep apnoea syndromes are the cause of their chronic symptoms of fatigue and memory and attentional disturbances.
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PMID:Sleep disturbances and occupational exposure to solvents. 1920 Dec 27

The proteinopathy sporadic Parkinson's disease (sPD) is the second most frequent degenerative disorder of the human nervous system after Alzheimer's disease. The alpha-synuclein inclusion body pathology (Lewy pathology) associated with sPD is distributed throughout the central, peripheral, and enteric nervous systems. The resulting nonrandom neuronal dysfunction and, in some regions, neuronal loss is reflected in a topographic distribution pattern of the Lewy pathology that, in the brain, can be staged. Except for olfactory structures and spinal cord constituents of the pain system, sensory components of the nervous system remain uninvolved or virtually intact. The most disease-related damage revolves around motor areas--particularly around superordinate centers of the limbic and visceromotor systems as well as portions of the somatomotor system. Vulnerable regions are interconnected anatomically and susceptible nerve cell types are not neurotransmitter-dependent. Not all clinical symptoms emerging in the course of sPD can be explained by a lack of dopamine in the nigrostriatal system. These include autonomic dysfunction, pain, hyposmia or anosmia, excessive daytime sleepiness, rapid eye movement (REM) sleep behavioral disorder, depression, anxiety, cognitive decline, and dementia. Against the background of the normal morphology and anatomy, the authors analyze the pathoanatomy of sPD in the nervous system at various neuropathological stages and summarize the potential functional consequences of the lesions.
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PMID:Neuroanatomy and pathology of sporadic Parkinson's disease. 1923 May 52

Kallmann syndrome is defined as a combination of isolated hypogonadotropic hypogonadism (IHH), hyposmia or anosmia and several optional neurological or anatomical particularities. The genetically caused illness affects mechanisms of neuronal migration, first of all concerning GnRH-producing neurons and those of the olfactory bulb.The first, nowadays rather seldom case, serves as an example of a patient suffering from grave, especially somatic symptoms of the disease. IHH, anosmia, eunuchoidism (physique, puerile voice, gynecomastia, micropenis, missing secondary sex characteristics) and distinct osteoporosis were verified.With the case of the second patient, late psychosexual sequelae of the syndrome are elucidated. The patient had been treated with testosterone after contracting mumps orchitis in early childhood. The physical development of the second patient progressed well since initiation of hormone substitution; however, infertility was still present. Now he complains of symptoms of depression caused by the separation from his female partner. Intermittent disorders of sexual functions and difficulties in establishing a male sexual identity lowered his self-esteem. Diagnostic and therapeutic capabilities and limits are particularized and items of future concern are emphasized.
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PMID:[Kallmann syndrome. Fundamentals and two medical histories]. 1950 27

We compared the relationship between regional cerebral blood flow (rCBF) of the olfactory area and the cognitive function and anosmia in patient with Parkinson disease (PD) and in those with Alzheimer disease (AD). UPDRS III, MMSE, HDS-R, CDR, Beck Depression Inventory (BDI) were employed in this study. The subjects included 56 PD patients (average age 71.4+/-9.69 years), 23 AD patients (average age 73.3+/-7.12 years), 12 patients with mild cognitive impairment (MCI) (average age 72.5+/-6.89 years), and 9 age-matched controls (NC) (average age 73.8+/-6.61 years). Next we intravenously injected 1 ampule of thiamine propyldisulphide (Alinamin) and confirmed anosmia. In addition, we performed 123I-IMP SPECT (SEE methods) and satistically determined rCBF of the olfactory area based on the basis of the Z scores of the interest area. Anosima was detected in approximately 40% of the PD and AD patients. The HDS-R and MMSE scores were significantly higher in patients with anosima than in those without anosima; the CDR scores were significantly higher in the former than in the latter. Further, the incidence of anosima in PD patients and AD patients with MCI increased with an increase in the CDR scores. In order to determine the rCBF of the olfactory area of the PD and AD patients. As to rCBF of the olfactory area, we examined left and right Z scores of hippocampus, parahippocampus, amygdala, and uncus at Talairach level 3 and the scores of the Brodmann area 28, 34, 35, and 36 at Talairach level 5. In patients with anosmia, the Z scores were significantly high in cases with anosmia in all areas except the right Brodmann area 34 in PD patients and the right Brodmann area 28 and bilateral the Brodmann area 34 of both sides in AD patients. Some parts of the olfactory area are closely related to cognitive function, and it appeares that a reduced rCBF in the olfactory areas may lead to a functional decline in these regions which may cause anosmia and cognitive decline in PD and AD patients.
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PMID:[Relationship between the regional cerebral blood flow and the cognitive function and anosmia in patients with Parkinson disease and Alzheimer disease]. 1952 36

Parkinson's disease (PD) is a progressive neurodegenerative disorder that is characterized by the loss of dopamine neurons in the substantia nigra pars compacta, culminating in severe motor symptoms, including resting tremor, rigidity, bradykinesia, and postural instability. In addition to motor deficits, there are a variety of nonmotor symptoms associated with PD. These symptoms generally precede the onset of motor symptoms, sometimes by years, and include anosmia, problems with gastrointestinal motility, sleep disturbances, sympathetic denervation, anxiety, and depression. Previously, we have shown that mice with a 95% genetic reduction in vesicular monoamine transporter expression (VMAT2-deficient, VMAT2 LO) display progressive loss of striatal dopamine, L-DOPA-responsive motor deficits, alpha-synuclein accumulation, and nigral dopaminergic cell loss. We hypothesized that since these animals exhibit deficits in other monoamine systems (norepinephrine and serotonin), which are known to regulate some of these behaviors, the VMAT2-deficient mice may display some of the nonmotor symptoms associated with PD. Here we report that the VMAT2-deficient mice demonstrate progressive deficits in olfactory discrimination, delayed gastric emptying, altered sleep latency, anxiety-like behavior, and age-dependent depressive behavior. These results suggest that the VMAT2-deficient mice may be a useful model of the nonmotor symptoms of PD. Furthermore, monoamine dysfunction may contribute to many of the nonmotor symptoms of PD, and interventions aimed at restoring monoamine function may be beneficial in treating the disease.
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PMID:Nonmotor symptoms of Parkinson's disease revealed in an animal model with reduced monoamine storage capacity. 1982 98

We report four cases of patients with clinically isolated apathy which was mistaken for depression even though they were suffering from voluminous brain tumors. These cases remind us that rigorous clinical analysis is essential: searching for signs of organic origin or psychiatric etiology is fundamental to avoid an incorrect diagnosis. In particular, these four patients displayed anosmia, an uncommon symptom for patients suffering from depression. In addition, brain imaging is important to correctly identify the most prudent medical and/or surgical management strategy. In this short discussion, we propose an algorithm for the clinical diagnosis of apathy.
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PMID:[Apathy or depression? Do you have a nose for it? Four case reports of paramedian frontal tumors]. 2043 45

Septoplasty is a common procedure in otolaryngology used to address nasal obstruction caused by a deviated nasal septum. It is often accompanied by inferior turbinate reduction. Complications that may arise from this procedure include excessive bleeding; cerebrospinal fluid rhinorrhea; extraocular muscle damage; wound infection; septal abscess; toxic shock syndrome; septal perforation; saddle nose deformity; nasal tip depression; and sensory changes, such as anosmia or dental anesthesia. Local and general anesthetics have been used to successfully perform septoplasty and the operation may be done either endoscopically or open. Overall, good intraoperative visualization is a key factor in preventing complications and achieving a functional nasal airway.
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PMID:Complications and management of septoplasty. 2059 92

Parkinson's disease is not only a movement disorder: non-motor symptoms such as loss of smell, constipation, depression, cognitive impairment, sleep problems and disturbances of the autonomic nervous system also feature. The etiology is still unknown, although an increasing number of gene-related Parkinsonian syndromes have been identified. It is intriguing to speculate that PD starts by the intake of a toxin, bacteria or virus. This idea stems from the fact that pathological abnormalities such as Lewy neuritis, Lewy bodies and alpha-synuclein accumulation are first found in the enteric nervous system of the gut and in the olfactory bulb. There is increasing evidence that the disease may spread out from the enteric nervous system of the gut via the vagal nerve up to the brain. Here we present data from animal work which supports this assumption.
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PMID:View point: etiology in Parkinson's disease. Dual hit or spreading intoxication. 2160 May 91


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