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)

Myoclonus-dystonia syndrome (MDS) is an autosomal dominant disorder characterized by myoclonic and dystonic muscle contractions, associated with psychiatric manifestations. MDS is usually considered as a benign disease. In most of the families, MDS is linked to chromosome 7q21 and mutations within epsilon-sarcoglycan (SGCE) gene have been recently described. We report a MDS family with a severe and heterogeneous phenotype, including myoclonus with important functional impact and several psychiatric features, characterized by obsessive-compulsive disorder, depression, and anxiety. This phenotype was shown to be associated with a novel truncating mutation located within exon 4 of SGCE.
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PMID:Severe myoclonus-dystonia syndrome associated with a novel epsilon-sarcoglycan gene truncating mutation. 1270 48

Psychogenic dystonia has been a controversial diagnosis over the past century. While this entity does exist, it makes up the minority of cases of dystonia seen at specialized centres. The diagnosis of psychogenic dystonia must only be undertaken by a neurologist with considerable experience in the assessment and treatment of organic dystonia. Features in the history and physical examination will reveal both clinical inconsistencies and incongruities with organic dystonia that support a psychogenic cause for the patient's symptoms. Patients with psychogenic dystonia suffer from motor conversion disorder, and co-morbid depression, anxiety and disorders of personality are frequent. While there have been no neuroimaging studies to date in patients with psychogenic dystonia, imaging studies in patients with organic dystonia offer insights on how one might assess this problem using functional neuroimaging. Neurophysiologic studies in patients with organic forms of dystonia may also be employed to further distinguish psychogenic from organic dystonia when doubt exists. The prognosis of psychogenic dystonia is disappointing, with the majority of patients suffering significant long-term disability. Recommendations are given regarding disclosure of the diagnosis of psychogenic dystonia to the patient as well as appropriate treatment.
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PMID:Psychogenic dystonia. 1461 77

The development of abnormal posturing of the neck or shoulder after local injury has been termed posttraumatic cervical dystonia (PTCD). Certain features seem to distinguish a unique subgroup of patients with this disorder from those with features more akin to typical idiopathic cervical dystonia, such as onset and maximum disability that occurs very quickly after injury, severe pain and a fixed abnormal posture. In an attempt to clarify the nature of this syndrome further, we evaluated 16 such patients (8 men, 8 women). Motor vehicle accident and work-related injuries were common precipitants, with posturing usually developing shortly after trauma, and little progression occurring after the first week. A characteristic, painful, fixed head tilt and shoulder elevation were present in all but one patient, who had a painless elevated shoulder and painful contralateral shoulder depression, as well as nondermatomal sensory loss in 14 patients. Additional abnormalities included dystonic posturing in a limb (2 patients) or jaw (1 patient), limb tremor (3 patients) and "give-way" limb weakness (8 patients). The tremor and the jaw dystonia demonstrated features suggestive of a psychogenic movement disorder, most commonly distractibility. Litigation or compensation was present in all 16 patients. Intravenous sodium amytal improved the posture, pain or both in 13 of 13 patients; in 7 of 13 the sensory deficit either markedly improved or normalized. General anesthesia demonstrated full range of motion in all 5 patients assessed. Psychological evaluations suggested that psychological conflict, stress, or both were being expressed via somatic channels in 11 of 12 tested patients. Our results suggest an important role of psychological factors in the etiology or maintenance of abnormal posture, pain and associated disability of these patients. The role of central factors triggered in psychologically vulnerable individuals after physical trauma is discussed. We propose that the disorder be referred to as "posttraumatic painful torticollis" rather than characterize it as a form of dystonia until further information on its pathogenesis is forthcoming.
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PMID:Posttraumatic painful torticollis. 1467 85

Interest in brain stimulation therapies has been rejuvenated over the last decade and brain stimulation therapy has become an alternative treatment for many neurological and psychiatric disorders, including Parkinson's disease (PD), dystonia, pain, epilepsy, depression, and schizophrenia. The effects of brain stimulation on PD are well described, and this treatment has been widely used for such conditions worldwide. Treatments for other conditions are still in experimental stages and large-scale, well controlled studies are needed to refine the treatment procedures. In the treatment of intractable brain disorders, brain stimulation, especially transcranial magnetic stimulation (TMS), is an attractive alternative to surgical lesioning as it is relatively safe, reversible, and flexible. Brain stimulation, delivered either via deeply implanted electrodes or from a surface-mounted transcranial magnetic device, can alter abnormal neural circuits underlying brain disorders. The neural mechanisms mediating the beneficial effects of brain stimulation, however, are poorly understood. Conflicting theories and experimental data have been presented. It seems that the action of stimulation on brain circuitry is not limited to simple excitation or inhibition. Alterations of neural firing patterns and long-term effects on neurotransmitter and receptor systems may also play important roles in the therapeutic effects of brain stimulation. Future research on both the basic and clinical fronts will deepen our understanding of how brain stimulation works. Real-time computation of neural activity allows for integration of brain stimulation signals into ongoing neural processing. In this way abnormal circuit activity can be adjusted by optimal therapeutic brain stimulation paradigms.
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PMID:Brain stimulation for neurological and psychiatric disorders, current status and future direction. 1473 4

The authors investigated the prevalence of DIS-ascertained DSM-III psychiatric disorders occurring in 28 patients with dystonia and 28 patients with Parkinson's Disease (PD). In patients with dystonia, lifetime prevalences of major depression (25.0%), bipolar disorder (7.1%), atypical bipolar disorder (7.1%), social phobia (17.9%), and generalized anxiety disorder (25.0%) were significantly more common than in epidemiologic catchment area (ECA) study population controls (p < 0.005). Social phobia and generalized anxiety disorder preceded dystonia (primary), while bipolar disorder developed after dystonia onset (secondary). In PD patients, the lifetime prevalence of simple phobia (35.7%, p < 0.0001) and atypical depression (21.4%) were significantly more common. Parkinson's Disease was associated with primary simple phobia and secondary atypical depression. These findings are considered in light of previous results and in terms of the differences in pallidothalamic physiologies in dystonia and PD. These data suggest distinctive profiles of psychiatric disorders in dystonia and PD.
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PMID:Differential DSM-III psychiatric disorder prevalence profiles in dystonia and Parkinson's disease. 1499 Jul 56

Post-traumatic cervical dystonia as a diagnostic entity remains a subject of debate. Patients with cervical dystonia (CD) were asked to identify any significant illness prior to the onset of their CD. Sixteen patients of 95 respondents reported a history of injury in the four-week period prior to onset of their dystonia. A retrospective study of the clinical characteristics of the 16 patients with early post-traumatic CD (CD-PT) in comparison with the 52 patients reporting no antecedent trauma (CD-NT) was performed. In this comparison the CD-PT group had a significantly increased frequency of laterocollis, significantly more reported pain and more reported depression. Non-significant trends were noted for less responsiveness to botulinum toxin and less use of gestes antagonistes in the CD-PT group. There were no group differences in the presence of a family history of dystonia. Eleven of the CD-PT group had been or were currently involved in litigation. A sub-group of seven CD-PT patients had laterocollis, six of whom conformed to a clinical pattern of persistent non-spasmodic laterocollis with marked pain; all seven had been involved in litigation. This form of CD-PT is a distinct clinical entity and has an onset within hours or a few days of the trauma. In contrast, no significant differences were noted between patients with CD-NT and the eight patients with later onset of CD between 4 weeks and one year after peripheral trauma.
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PMID:Cervical dystonia following peripheral trauma--a case-control study. 1499 48

High-frequency deep brain stimulation (DBS) of the thalamus or basal ganglia represents an effective clinical technique for the treatment of several medically refractory movement disorders (e.g., Parkinson's disease, essential tremor, and dystonia). In addition, new clinical applications of DBS for other neurologic and psychiatric disorders (e.g., epilepsy and obsessive-compulsive disorder) have been vaulted forward. Although DBS has been effective in the treatment of movement disorders and is rapidly being explored for the treatment of other neurologic disorders, the scientific understanding of its mechanisms of action remains unclear and continues to be debated in the scientific community. Optimization of DBS technology for present and future therapeutic applications will depend on identification of the therapeutic mechanism(s) of action. The goal of this review is to address the present knowledge of the effects of high frequency stimulation within the central nervous system and comment on the functional implications of this knowledge for uncovering the mechanism(s) of DBS. Four general hypotheses have been developed to explain the mechanism(s) of DBS: depolarization blockade, synaptic inhibition, synaptic depression, and stimulation-induced modulation of pathologic network activity. Using the results from microdialysis, neural recording, functional imaging, and neural modeling experiments, the authors address the main hypotheses and attempt to reconcile what have been considered conflicting results from different research modalities.
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PMID:How does deep brain stimulation work? Present understanding and future questions. 1509 93

Adult-onset focal dystonia was the presenting sign of pantothenate kinase-associated neurodegeneration (PKAN) in a patient with a novel homozygous missense mutation (C856T). His brother shared the same mutation and showed similar, albeit minor, motor signs, but a different behavioral profile. Both brothers had an atypical form of PKAN. The neuropsychological assessment showed that, despite a normal Mini-Mental State Examination, both patients presented a deficit of executive functions and of attention. The profile of cognitive impairment in these cases was typically that of a subcortical dementia. Both patients fulfilled Diagnostic and Statistical Manual for Mental Disorders criteria for obsessive-compulsive disorder; however, paranoia was associated with depression and aggressive behavior in Patient 1, whereas Patient 2 had hyperactivity, disinhibition, and euphoria. Our findings suggest that these two brothers had a different pattern of involvement of motor and nonmotor basal ganglia-thalamocortical circuits.
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PMID:Clinical and neuropsychological correlates in two brothers with pantothenate kinase-associated neurodegeneration. 1539 30

The purpose of this study is to determine the prevalence and the patterns of movement disorders (MD) in outpatients submitted to the chronic use of cinnarizine (cz) or flunarizine (fz), and to establish the main risk factors for MD development. Over a period of 3 months, data were collected from outpatients who were chronic users of cz or fz in a municipal health institute. A total of 26 outpatients were included and all of them were submitted to a protocol that included DSM-4 diagnosis criteria for drug-induced movement disorders, parkinsonism (PK) and depression. Parkinsonism was diagnosed in 34% of the patients, PK plus akathisia, PK plus akathisia and bucco-linguo-masticatory syndrome (BLMS), isolated BLMS and dystonia were found in 4% patients each. Patients with BLMS had the highest median age and the longest average period in which they used the drugs. The affected group, when compared to the non-affected one, presented with higher rates of depression. This study demonstrates the existence of a direct relationship between the time of use of cz and fz, the age and the prevalence of PK and other MD. It also suggests that these drugs increase the incidence of depression.
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PMID:Parkinsonism and other movement disorders in outpatients in chronic use of cinnarizine and flunarizine. 1547 69

Nocturnal disturbances are common in Parkinson's disease (PD) patients, with almost 70% of these patients reporting nocturnal disturbances. The etiology of sleep disturbances in patients with PD is still controversial. They might be dependent on dopaminergic drugs, on disease progression, or on a combination of these two factors. Nocturnal disturbances can be categorized in four groups: 1) PD-related motor symptoms, including nocturnal akinesia, early-morning dystonia, painful cramps, tremor, and difficulty turning in bed; 2) treatment-related nocturnal disturbances; 3) psychiatric symptoms, including hallucinations, vivid dreams, depression, dementia, insomnia, psychosis, and panic attacks; 4) other sleep disorders, including insomnia, REM behavioral disorder (RBD), restless legs syndrome (RLS), periodic leg movements (PLMS), and excessive daytime sleepiness (EDS). Specific treatment options are supplied for every group. A global evaluation of nocturnal disturbances would provide clinicians with a valuable tool to establish an optimal regimen that could positively influence all nocturnal disturbance categories and thus improve PD management on. However, it is important to consider that management of some nocturnal disturbances in a group may worsen nocturnal symptoms of another group or may increase EDS. PD-related symptoms can be treated with long-acting DA agonists to obtain continuous DA receptor stimulation during the night. Both treatment-related nocturnal disturbances and psychiatric symptoms may be related to drug treatment, and therefore, in both cases, drug reduction or discontinuance should be considered. Some sleep disorders, such as RLS and PLMS, may be controlled by DA agents, and others, such as insomnia and EDS, may be improved by reducing dopaminergic stimulation.
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PMID:Treatment of nocturnal disturbances and excessive daytime sleepiness in Parkinson's disease. 1550 42


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