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)

We sought to review the long-term tolerability of tetrabenazine (TBZ) and seek determinants of tolerability in the treatment of hyperkinetic movement disorders. A retrospective chart review was performed on patients treated with TBZ between 1997 and 2004. Efficacy of TBZ was assessed by a 1- to 5-point response scale (1 = marked reduction in abnormal movements, 5 = worsening). All adverse events (AEs) were captured according to their relationship with study drug. A total of 448 patients (42% male) were treated for a variety of hyperkinesias, including tardive dyskinesia (n = 149), dystonia (n = 132), chorea (n = 98), tics (n = 92), and myoclonus (n = 19). The mean age at onset of the movement disorder was 43.0 +/- 24.2 years, with TBZ starting at a mean age of 50.0 +/- 22.3 years. Patients remained on treatment for a mean of 2.3 +/- 3.4 years. An efficacy response rating of 1 or 2 was sustained in the majority of patients between the first and last visit. Common AEs included drowsiness (25.0%), Parkinsonism (15.4%), depression (7.6%), and akathisia (7.6%). Comparison of log-likelihood ratios revealed that age was a reliable predictor of Parkinsonism (P < 0.0001). TBZ is a safe and effective drug for the long-term treatment of hyperkinetic movement disorders.
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PMID:Long-term tolerability of tetrabenazine in the treatment of hyperkinetic movement disorders. 1713 12

We describe two affected individuals in a family with myoclonus-dystonia syndrome complicated with severe depression. One individual committed suicide. Molecular genetic analysis revealed a heterozygous point mutation in the epsilon-sarcoglycan gene, which we show leads to skipping of exon 5. This report suggests that the psychiatric spectrum of MDS includes more severe depression.
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PMID:Myoclonus-dystonia syndrome with severe depression is caused by an exon-skipping mutation in the epsilon-sarcoglycan gene. 1723 Apr 65

This review focuses on sensory information originating from muscle spindles and its role in proprioception and motor control. The first part reminds of the structural and functional properties of these muscle mechanoreceptors, with arguments for an independent fusimotor command, i.e. the gamma-motoneurons, that would regulate spindle mechanical sensitivity in keeping with the requirements of ongoing motor action. The possibility that dysfunction of the fusimotor system might be responsible for clinical signs is discussed with respect to the hyperexcitability of the sensorimotor cortex that is observed in myoclonus of cortical origin. What is known about the spindle afferents projections into the spinal cord and about the dysfunction of the spinal sensorimotor networks in patients with neurological disorders, is put together in the second part. It is stressed on the significant complexity of the monosynaptic reflex in spite of its "simple" organization. The monosynaptic reflex constitutes the only possible way for testing the excitability of motoneurons and spinal networks. This method is extensively used clinically to examine changes in the nervous system with diseases. When studying changes from the norm, it is important to understand how the reflex functions in neurologically normal conditions. Different mechanisms such as pre-synaptic inhibition, post-activation depression and motoneuronal intrinsic properties are reviewed as they may induce changes in reflex amplitude and have therefore consequences for interpretation of spinal excitability.
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PMID:Proprioception and myoclonus. 1733 74

We report two cases of serotonin syndrome in elderly patients during treatment of psychotic depression with atypical antipsychotics and antidepressants. The first case is a 69-year-old man who was admitted for depression with psychosis and treated with trazodone, risperidone, and sertraline. Subsequently, he developed myoclonus, tremor, cogwheel rigidity, and diaphoresis. The second case is a 72-year-old female initially admitted to a medical inpatient unit for a change in mental status that presented as increased confusion, lethargy, slurred speech, and a fever of 101.5 degrees. She had been on phenelzine and quetiapine. In both cases, all symptoms resolved within 24 hours of the psychotropics being stopped. In both cases, we believe that serotonin syndrome was produced by a combination of an antidepressant and an atypical antipsychotic. There have been several case reports of serotonin syndrome from similar combinations of antidepressant and atypical antipsychotic treatment. Clinicians treating elderly patients with a combination of serotonergic antidepressants and atypical antipsychotics for psychotic depression should be aware of the potential for serotonin syndrome.
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PMID:Serotonin syndrome in elderly patients treated for psychotic depression with atypical antipsychotics and antidepressants: two case reports. 1766 87

The epilepsies are among the most common serious brain disorders, can occur at all ages, and are characterized by a variety of presentations and causes. Diagnosis of epilepsy remains clinical, and neurophysiological investigations support the diagnosis of the syndrome. Brain imaging is able to identify many of the structural causes of the epilepsies. Current antiepileptic drugs (AEDs) block seizures without influencing the underlying tendency to generate seizures, and are effective in 60-70% of individuals. Several modern drugs are as efficacious as the older medications, but have important advantages including the absence of adverse drug interactions and hypersensitivity reactions. Epilepsy is associated with an increased prevalence of mental health disorders including anxiety, depression, and suicidal thoughts. An understanding of the psychiatric correlates of epilepsy is important to the adequate management of people with epilepsy. Anticipation of common errors in the diagnosis and management of epilepsy is important. Frequent early diagnostic errors include nonepileptic psychogenic seizures, syncope with myoclonus, restless legs syndrome, and REM behavioral disorders, the last mostly in elderly men. Overtreatment with too rapid titration and too high doses or too many AEDs should be avoided. For people with refractory focal epilepsy, vagus nerve stimulation offers palliative treatment with possible mood improvement and neurosurgical resection offers the possibility of a life-changing cure. Potential advances in the management of epilepsy are briefly discussed. This short review summarizes the authors' how-to-do approach to the modern management of people with epilepsy.
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PMID:Modern management of epilepsy: a practical approach. 1831 96

Unverricht-Lundborg disease (ULD), progressive myoclonic epilepsy type 1 (EPM1, OMIM254800), is an autosomal recessively inherited neurodegenerative disorder characterized by age of onset from 6 to 16 years, stimulus-sensitive myoclonus, and tonic-clonic epileptic seizures. Some years after the onset ataxia, incoordination, intentional tremor, and dysarthria develop. Individuals with EPM1 are mentally alert but show emotional lability, depression, and mild decline in intellectual performance over time. The diagnosis of EPM1 can be confirmed by identifying disease-causing mutations in a cysteine protease inhibitor cystatin B (CSTB) gene. Symptomatic pharmacologic and rehabilitative management, including psychosocial support, are the mainstay of EPM1 patients' care. Valproic acid, the first drug of choice, diminishes myoclonus and the frequency of generalized seizures. Clonazepam and high-dose piracetam are used to treat myoclonus, whereas levetiracetam seems to be effective for both myoclonus and generalized seizures. There are a number of agents that aggravate clinical course of EPM1 such as phenytoin aggravating the associated neurologic symptoms or even accelerating cerebellar degeneration. Sodium channel blockers (carbamazepine, oxcarbazepine) and GABAergic drugs (tiagabine, vigabatrin) as well as gabapentin and pregabalin may aggravate myoclonus and myoclonic seizures. EPM1 patients need lifelong clinical follow-up, including evaluation of the drug-treatment and comprehensive rehabilitation.
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PMID:Clinical picture of EPM1-Unverricht-Lundborg disease. 1832 13

Medications which bind to opioid receptors are increasingly being prescribed for the treatment of multiple and diverse chronic painful conditions. Their use for acute pain or terminal pain is well accepted. Their role in the long-term treatment of chronic noncancer pain is, however, controversial for many reasons. One of the primary reasons is the well-known phenomenon of psychological addiction that can occur with the use of these medications. Abuse and diversion of these medications is a growing problem as the availability of these medications increases and this public health issue confounds their clinical utility. Also, the extent of their efficacy in the treatment of pain when utilized on a chronic basis has not been definitively proven. Lastly, the role of opioids in the treatment of chronic pain is also influenced by the fact that these potent analgesics are associated with a significant number of side effects and complications. It is these phenomena that are the focus of this review. Common side effects of opioid administration include sedation, dizziness, nausea, vomiting, constipation, physical dependence, tolerance, and respiratory depression. Physical dependence and addiction are clinical concerns that may prevent proper prescribing and in turn inadequate pain management. Less common side effects may include delayed gastric emptying, hyperalgesia, immunologic and hormonal dysfunction, muscle rigidity, and myoclonus. The most common side effects of opioid usage are constipation (which has a very high incidence) and nausea. These 2 side effects can be difficult to manage and frequently tolerance to them does not develop; this is especially true for constipation. They may be severe enough to require opioid discontinuation, and contribute to under-dosing and inadequate analgesia. Several clinical trials are underway to identify adjunct therapies that may mitigate these side effects. Switching opioids and/or routes of administration may also provide benefits for patients. Proper patient screening, education, and preemptive treatment of potential side effects may aid in maximizing effectiveness while reducing the severity of side effects and adverse events. Opioids can be considered broad spectrum analgesic agents, affecting a wide number of organ systems and influencing a large number of body functions.
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PMID:Opioid complications and side effects. 1844 35

Insomnia and depression are frequently encountered in patients during withdrawal from substances. While there are no approved medications for treating them, off-label attempts to address these phenomena with mirtazapine have shown some promising results. This case describes the use of mirtazapine as an aid in benzodiazepine withdrawal and its potential benefits in alleviating insomnia and depression in a 32-year-old man. It was found to ameliorate sleep myoclonus that was thought to be associated with his withdrawal syndrome. It is hoped this report will generate interest and stimulate further research in this area of psychopharmacology.
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PMID:Employing mirtazapine to aid benzodiazepine withdrawal. 1858 Oct 12

The aims of this study were to clarify if patients with Unverricht-Lundborg disease (ULD) have adequate cognitive functioning and to delineate their neuropsychological profile. We evaluated 20 patients with ULD and 20 healthy, matched controls. Mean age of the patients was 35 years, and mean duration of disease, 22 years. Patients underwent a neuropsychological battery exploring intelligence, executive functions, visuospatial and verbal memory, depression, and anxiety. Eleven of 20 subjects with ULD had mild to moderate cognitive impairment. Compared with controls, patients with ULD had lower scores on all short-term memory and executive function tasks. Linear regression analysis disclosed significant associations between impaired performance on some memory tests and duration of disease and between severity of myoclonus and performance on most executive function tests. In conclusion, most patients with ULD seem to be impaired with respect to cognitive abilities. Longitudinal prospective studies are needed to confirm and further expand our findings.
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PMID:Neuropsychological findings in patients with Unverricht-Lundborg disease. 1918 15

Propofol is now the most commonly used intravenous anesthetic-for general anesthesia and sedation because of its rapid onset and recovery. Besides the well-known adverse effects of cardiovascular and respiratory depression, recent studies indicate that propofol may cause excitatory phenomena such as myoclonus, opisthotonus, and even seizure. However, the mechanisms of these excitatory effects of propofol have not been elucidated. Considering glutamate as the principle excitatory neurotransmitter in the central nervous system and excessive glutamatergic synaptic transmission can cause seizure, we examined the effect of propofol on the release of glutamate from rat cerebral cortex nerve terminals (synaptosomes). Results showed that subanesthetic concentration propofol facilitated 4-aminopyridine (4-AP), but not KCl- or ionomycin-evoked glutamate release from nerve terminals. The facilitation of 4-AP-evoked glutamate release by propofol also occurred in the calcium chelation and significantly attenuated by glutamate transporter inhibitors, DL-threo-beta-benzyloxyaspartic acid (DL-TBOA) and L-trans-pyrrolidine-2,4-dicarboxylic acid (L-trans-PDC). In addition, propofol increased 4-AP-evoked depolarization of the plasma membrane potential. Furthermore, protein kinase C (PKC) inhibition suppressed propofol-mediated facilitation of glutamate release. These results suggest that subanesthetic concentration propofol facilitates glutamate release from rat cerebrocortical glutamatergic terminals by increasing nerve terminal excitability, likely through the activation of PKC pathway. This finding may provide an explanation for propofol-induced excitatory phenomena.
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PMID:Facilitation of glutamate release from rat cerebral cortex nerve terminal by subanesthetic concentration propofol. 1948 7


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