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

The use of tetrabenazine to treat the movement disorder of Huntington's chorea and other dyskinesias is described. Tetrabenazine produced moderate to marked improvement in the movement disorder in 79% of a series of 40 Australian patients. The most commonly reported side effects were depression, drowsiness and Parkinsonism.
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PMID:Tetrabenazine for involuntary movement disorders. 15

A 62-year-old woman developed neurologic deficits 7 months after pulmonary lobectomy for alveolar cell carcinoma of the lung. CT scan of the head demonstrated two metastases with marked peritumoral edema. Administration of Decadron, chemotherapy and 3,000 rad cranial radiation resulted in dramatic improvement of dysphasia and right hand paresis. Almost 2 months later, rhythmic, involuntary movements of the left hand developed. There was progression to multifocal seizures, grand mal seizures, postictal depression, status epilepticus, and coma, with death 9 days after onset of the movement disorder. Bronchoalveolar carcinoma was widely disseminated in lungs and bones, and as three metastases in brain. Bland "ischemic" necrosis in a pseudolaminar pattern was present in the neocortex. Innumerable Cowdry type A intranuclear inclusion bodies were seen in neurons, astrocytes, and oligodenodroglia. Immunofluorescence demonstrated Herpes simplex virus type 2 antigen and electron microscopy revealed virions with the morphology of the Herpes group. The case is significant for (1) the concurrence of intracranial metastases and Herpes simplex encephalitis, and (2) the causal agent, Herpes simplex virus type 2. The implication for the clinical neurocientist is the potential in a patient with systemic cancer, for the causation of neurologic complications by more than one factor or mechanism.
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PMID:Herpes simplex type 2 encephalitis concurrent with known cerebral metastases. 22 22

Patients with depressive motor retardation, neuroleptic induced parkinsonism or Parkinson's disease were tested on movement tasks requiring control of simultaneous movements. This was in order to determine whether these three groups of patients, who all show slowing of movements, also share the distinctive impairment of simultaneous movement control that is observed in Parkinson's disease. Though all three patient groups showed equivalent slowing on the motor tasks that were studied, the patterns of impairment were different. Only the patients with parkinsonism, either neuroleptic induced or from Parkinson's disease, showed additional slowing of a rapid ballistic elbow flexion movement when it was performed simultaneously with a rapid squeeze of the ipsilateral hand. Only patients with parkinsonism showed a significant increase in dual task interference on a bimanual bead and tapper task, compared with controls. The bead and tapper interference in patients with depressive motor retardation was between that of controls and parkinsonism. Having a bimanual skill had a large effect on the subjects' dual task interference on this task. The measures of dual task interference for the two tasks did not correlate with one another; difficulty running simultaneous motor programs does therefore not explain the interference that is observed when tapping is performed while the other hand simultaneously performs a dextrous motor task. Only patients with parkinsonism showed increased fatigue on the tapping task. The patients with depressive motor retardation did have elevated scores on a clinical rating of parkinsonism. Nevertheless there are clearly defined differences between the movement disorder observed in patients with depression, and that observed in in parkinsonism. The patterns of impairments in patients with neuroleptic parkinsonism were very similar to those of Parkinson's disease.
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PMID:Control of simultaneous movements distinguishes depressive motor retardation from Parkinson's disease and neuroleptic parkinsonism. 135 98

All cases (86) of Huntington's Disease presenting between 1970 and 1987 in the Grampian Health Board region were identified and a case note analysis of neurological and psychiatric syndromes carried out--the latter using the PSE syndrome check-list. The commonest syndromes were organic impairment, irritability, loss of interest and concentration and simple depression and these were often the presenting psychiatric syndromes. General anxiety, worrying and social unease occurred early, commonly before movement disorder and were associated with longer survival.
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PMID:The clinical manifestation of mental disorder in Huntington's disease: a retrospective case record study of disease progression. 182 3

Nineteen cases are described, including 12 cases from three different families and 7 nonfamilial cases, in which multisystem neurological disease was associated with acanthocytosis in peripheral blood and normal plasma lipoproteins. Mild acanthocytosis can easily be overlooked, and scanning electron microscopy may be helpful. Some neurologically asymptomatic relatives with significant acanthocytosis were identified during family screening, including some who were clinically affected. The mean age of onset was 32 (range 8-62) yrs and the clinical course was usually progressive but there was marked phenotypic variation. Cognitive impairment, psychiatric features and organic personality change occurred in over half the cases, and more than one-third had seizures. Orofaciolingual involuntary movements and pseudobulbar disturbance commonly caused dysphagia and dysarthria that was sometimes severe, but biting of the lips or tongue was rarely seen. Chorea was seen in almost all symptomatic cases but dystonia, tics, involuntary vocalizations and akinetic-rigid features also occurred. Two cases had no movement disorder at all. Computerized tomography often demonstrated cerebral atrophy. Caudate atrophy was seen less commonly, and nonspecific focal and symmetric signal abnormalities from the caudate or lentiform nuclei were seen by magnetic resonance imaging in 3 out of 4 cases. Depression or absence of tendon reflexes was noted in 13 cases and neurophysiological abnormalities often indicated an axonal neuropathy. Sural nerve biopsies from 3 cases showed evidence of a chronic axonal neuropathy with prominent regenerative activity, predominantly affecting the large diameter myelinated fibres. Serum creatine kinase activity was increased in 11 cases but without clinical evidence of a myopathy. Postmortem neuropathological examination in 1 case revealed extensive neuronal loss and gliosis affecting the corpus striatum, pallidum, and the substantia nigra, especially the pars reticulata. The cerebral cortex appeared spared and the spinal cord showed no evidence of anterior horn cell loss. Two examples of the McLeod phenotype, an X-linked abnormality of expression of Kell blood group antigens, were identified in a single family and included 1 female. The genetics of neuroacanthocytosis are unclear and probably heterogeneous, but the available pedigree data and the association with the McLeod phenotype suggest that there may be a locus for this disorder on the short arm of the X chromosome.
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PMID:Neuroacanthocytosis. A clinical, haematological and pathological study of 19 cases. 199 79

Huntington's disease (HD) is an inherited neuropsychiatric degenerative process characterized by movement disorder, dementia, and, often, affective disorder (AfD) (seen in 38% of patients). Depression in HD is not just an understandable reaction to fatal illness: 10% of HD patients develop mania; AfD can occur 20 yr before neurological signs; and mood disorders are not randomly distributed, but occur in a subset of HD families. This evidence suggests that AfD in HD relates to brain pathophysiology. With its clear neuropathology, HD is proposed as one model for biological underpinnings of idiopathic AfD. There is striking atrophy and neuronal loss in HD neostriatum, particularly caudate. Caudate has rich connections to the limbic system. It is hypothesized that AfD in HD relates to dysfunction of the part of the neostriatum damaged earliest, dorsal medial caudate. Preliminary studies on neuropathological differences between HD patients with and without AfD are discussed. HD neurochemistry is reviewed, emphasizing the excitotoxin hypothesis, which involves dysfunction of the glutamate neurotransmitter system in HD (especially the NMDA receptor, which contains a channel with a phencyclidine (PCP) binding site). Based on the HD model, it is suggested that the glutamate system (particularly NMDA receptors) be examined in idiopathic AfD.
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PMID:Huntington's disease as a model for mood disorders. Clues from neuropathology and neurochemistry. 214 28

The movement disorder investigated in these studies has some features in common with human idiopathic dystonia, and information obtained in these studies may be of potential clinical benefit. The present experimental results indicated that peptidergic stimulation of the LC resulted in a NE-mediated inhibition of cerebellar Purkinje cells located at terminals of the ceruleo-cerebellar pathway. However, it is not certain as to the following: (a) what receptors were stimulated by the ACTH N-terminal fragments at the LC that resulted in this disorder; (b) whether NE, released onto Purkinje cell synapses located at terminals of the ceruleo-cerebellar pathway, did indeed cause the long-term depression at Purkinje cell synapses (previously described by others) that resulted in the long duration of the movement disorder; (c) whether the inhibition of inhibitory Purkinje cells resulted in disinhibition or increased excitability of the unilateral cerebellar fastigial or interpositus nuclei, the output targets of the Purkinje cell axons, that may have been an important contributing factor to this disorder. These questions are currently being investigated.
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PMID:A dystonia-like syndrome after neuropeptide (MSH/ACTH) stimulation of the rat locus ceruleus. 284 Aug 7

Functional disability in Huntington's disease usually results from a combination of the movement disorder, intellectual decline, and psychopathological changes, but the unique contribution of each element has never been investigated. The Shoulson-Fahn functional capacity rating scale measures independence in such daily activities as eating, dressing, and managing personal finances, and is used to stage the illness and follow its progression. To determine which problems contribute most to reduced functional capacity as the disease evolves, we reviewed the records of 48 consecutive patients who were evaluated for intellectual and emotional status and motor disability. Each patient was staged and rated for functional capacity at the time of the examinations. Thirty-three of these patients were followed over several years with repeat evaluations at 6-month intervals. Intellectual impairment and depression correlated significantly with reduced functional capacity. However, when the somatic symptoms of depression were eliminated from the analysis, its relationship to functional capacity was no longer significant. Duration of illness, motor disability, and age at onset also had little impact. Neuropsychological test performance and functional capacity deteriorated over time. Our data suggest that intellectual impairment is a major factor in reducing functional capacity in the early stages of Huntington's disease.
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PMID:Correlates of early disability in Huntington's disease. 294 92

A 65-year-old woman with bipolar disorder and complicated cardiovascular disease who was on maintenance lithium therapy developed a movement disorder following high doses of trazodone for treatment of an acute depression. When the trazodone was reduced, the involuntary movements promptly ceased. Although the movement disorder could not with certainty be attributed to trazodone alone, the drug at least acted as an eliciting agent.
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PMID:The elicitation of a movement disorder by trazodone: case report. 406 20

Depression, anhedonia, state anxiety (A-state), trait anxiety (A-trait), and self-reported pain estimate were measured in almost 500 facial pain patients. These patients were divided into 3 diagnostic categories: myofacial pain dysfunction syndrome (MPD) [18], arthritis of the temporomandibular joints (TMJ arthritis), and trigeminal neuralgia. Three control groups were measured for comparison. They consisted of an normal, or non-patient group, a group of arthritis patients, and a group of movement disorder patients attending a neurology clinic. Among the facial pain patients and the normal controls few differences were found with regard to anhedonia and depression, The arthritis and neurology patients produced significantly higher depression and anhedonia scores than did several of the facial pain groups. Pain estimate ranged from 0 for control, to a mean of 67.6 +/- 31.3 for the trigeminal neuralgia patients with the MPD (means = 56.2 +/- 32.5) and the TMJ arthritis patients (means = 46.7 +/- 30.8) somewhat lower. Clinical variables such as duration of pain, help seeking behavior and total number of symptoms were correlated with depression but not with anhedonia scores, It is hypothesized that anhedonia is a measure separate from depression and may be more closely linked to suffering behavior that to pain behavior. Psychological variables did not discriminate among facial pain patients and in particular did not distinguish between so-called functional and organic illness.
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PMID:Depression, anhedonia and anxiety in temporomandibular joint and other facial pain syndromes. 730 2


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