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)

Three cases in which the signs and symptoms of Chiari I malformation were induced and worsened after the occurrence of supratentorial mass lesions are reported. The symptoms improved markedly after removal of the supratentorial lesions in these cases. In the first case, a meningioma in the right parietal region coexisted with Chiari I malformation. Although the cerebellar ataxia and nystagmus disappeared after tumor removal, decompressive surgery for the malformation was performed because of upper cervical nerve symptoms and the patient recovered completely. In the second case, the symptoms first occurred after a car accident, and a computed tomographic scan revealed not only a subdural hematoma, but also tonsillar herniation due to Chiari I malformation. After evacuation of the hematoma and decompressive surgery on the craniospinal junction, the symptoms disappeared. In the third case, the symptoms of malformation developed gradually with depression and gait disturbance. A meningioma in the left frontal region coexisted with Chiari I malformation. Although the symptoms improved remarkably after tumor removal, decompressive surgery on the craniospinal junction was performed because of upper cervical nerve symptoms, and the patient recovered completely. These clinical findings indicate that a supratentorial mass lesion may provoke the symptoms of Chiari I malformation in the aged.
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PMID:Is Chiari I malformation in the aged initiated by mechanical factors? Report of three cases. 169 48

The serum magnesium levels of all 12 allogeneic bone-marrow transplant recipients who experienced the neurotoxic effects of cyclosporin (CyA) were more than two standard deviations below the normal range. The neurological events seemed to segregate into three separate syndromes. 7 patients had grand-mal seizures, which occurred within the first several weeks of CyA therapy (median onset 12 days). At the time of their first seizure all 7 patients had hypomagnesaemia, which had developed rapidly over the preceding 1-3 weeks. 3 patients had four episodes of cerebellar ataxia, tremor, and depression. These subacute episodes developed after prolonged CyA therapy (median onset 67 days). Each episode was associated with hypomagnesaemia. 2 patients had a transient episode of expressive aphasia following a long period of hypomagnesaemia. In all cases symptoms resolved or did not recur with adequate magnesium replacement. These data suggest that CyA neurotoxicity is associated with hypomagnesaemia and may be treated or prevented with magnesium replacement.
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PMID:Association between cyclosporin neurotoxicity and hypomagnesaemia. 615 Jan 82

We report on a Spanish family with cooccurrence of manic-depression and a form of hereditary cerebellar ataxia. All affected individuals in the second generation showed cerebellar ataxia and manic-depression simultaneously. Since anticipation has been described in both disorders and the pattern of segregation may be autosomal as well as X-linked, we have searched for a possible involvement of two candidate genes which are located either on an autosome (SCA1) or on the X-chromosome (GABRA3). We concluded that expansion of trinucleotide repeats at SCA1 gene cannot be considered as a disease-causing mutation, and this gene should be initially discarded.
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PMID:Familial cosegregation of manic-depressive illness and a form of hereditary cerebellar ataxia. 757 72

We have investigated a 15 year old girl with progressive external ophthalmoplegia, including bilateral ptosis and retinal rod and cone cell dysfunction with atypical retinal pigmentation, complicated by cerebellar ataxia, partial cardiac conduction block, and diabetes mellitus. In infancy she had a severe crisis of bone marrow depression, and as a child she suffered from hypersensitivity to light, increasing fatigue, and vertigo, signs that were initially though to be psychosomatic. Histological examination showed mitochondrial myopathy, and subsequent mitochondrial DNA (mtDNA) analysis showed a deletion of approximately 5500 base pairs in 35 to 40% of her muscle mtDNA. We therefore conclude that this patient has developed the Kearns-Sayre syndrome after a Pearson syndrome-like crisis in her first year of life.
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PMID:Juvenile Kearns-Sayre syndrome initially misdiagnosed as a psychosomatic disorder. 815 37

A large Swedish family with members affected by progressive external ophthalmoplegia with hypogonadism were followed-up and reviewed. Hypogonadism included delayed sexual maturation, primary amenorrhea, early menopause, and testicular atrophy. Cataracts, cerebellar ataxia, neuropathy, hypoacusia, pes cavus, tremor, parkinsonism, depression, and mental retardation were other features observed in this family. Muscle biopsy samples of advanced cases showed ragged-red fibers, focal cytochrome c oxidase deficiency, and multiple mtDNA deletions by Southern blot analysis. An autosomal dominant mode of inheritance was evident with anticipation in successive generations. Linkage analysis excluded the chromosome 10q23.3-q24.3 region reported as being linked to the disease in a Finnish family with autosomal dominant progressive external ophthalmoplegia. We report for the first time clinical evidence for anticipation in a family with autosomal dominant progressive external ophthalmoplegia. We hypothesize that the nuclear gene causing this enigmatic disorder may be directly influenced by an expansion of an unstable DNA sequence and that the resulting phenotype is caused by a concerted action with multiple deletions of mtDNA.
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PMID:Anticipation of autosomal dominant progressive external ophthalmoplegia with hypogonadism. 894 Dec 70

Analysis of the neuropathological mutant animals offers us great information on the development and differentiation of the nervous system. I have here introduced two examples of the analyses of the various kinds of neuropathological mutant mice. First one is the mutant mice where Purkinje neurons in the cerebellum are absent. High molecular weight protein, P400, enriched in the Purikinje cells in the cerebellum was greatly decreased in the Purkinje cell deficient mutant mice, nervous, pcd, Lurcher. We demonstrated that P400 is equivalent to IP3 receptor type 1. We found that IP3 receptor type 1 plays an important role in Ca2+ wave in fertilization and long term depression in the cerebellum which is one of the typical example of neuronal plasticity in the cerebellum. Second mutant is reeler mice where neuronal positioning in the brain is abnormal. We found CR50 antigen, reelin is the key molecule as a secreted molecule from Cajal-Retzius neuron for the neuronal positioning. We produced IP3 receptor deficient mice by gene targeting. The birth rate was one fifth of the control and the animals die before 25 postnatal days. They showed cerebellar ataxia and epileptic seizure.
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PMID:[Molecular biological analysis of the development of the mammalian central nervous system]. 957 52

In paralytic shellfish poisoning a mollusc contaminated with a toxin (saxitoxin) causes a potentially lethal disease, clinically characterised by gastrointestinal and neurological symptoms, of which possible respiratory depression is the most serious. The toxin acts by blocking the sodium channels. We report 9 Portuguese patients with this disease. The mollusc was identified as Mytilus edulis, contaminated with the dinoflagellate Gymnodinium catenatum, and the toxin saxitoxin. Our patients had a benign clinical course with cerebellar ataxia as the most severe neurological impairment. Eight out of 9 patients had neurophysiological investigations, the largest number so far reported. Motor and sensory conduction velocities and amplitudes were normal. The proximal conduction times, as assessed by F waves, showed delayed conduction and decreased frequency, which returned to normal in few weeks. The somatosensory evoked potentials confirmed normal peripheral and central sensory conduction. The rich vascular supply at root level of the sodium channels of the proximal motor nerves may explain the greater vulnerability to toxin damage. The typically transient and quickly reversible nerve dysfunction caused by ion channel blockade is reported.
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PMID:Paralytic shellfish poisoning: clinical and electrophysiological observations. 974 20

Humoral immune response to glutamic acid decarboxylase (GAD) has been implicated in the pathogenesis of stiff-man syndrome and cerebellar ataxia, but the underlying pathomechanism is unclear. Using a whole-cell patch-clamp technique with rat cerebellar slices, we found that immunoglobulins present in the cerebrospinal fluid of an ataxic patient acted presynaptically to cause a selective suppression of GABAergic transmission. This synaptic depression was most likely elicited by an autoantibody to GAD.
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PMID:Selective suppression of cerebellar GABAergic transmission by an autoantibody to glutamic acid decarboxylase. 1044 95

Ramsay Hunt syndrome (RHS) is a rare condition within the progressive myoclonic epilepsies syndrome (PME), with a triad of action myoclonus, grand mal seizure and severe cerebellar ataxia. There are few reports about the psychiatric disturbances associated with PME or RHS. The present study examines the evidence that RHS may accompany an organic mental syndrome, ethanol's effective suppression of myoclonus, and the possible resultant problem of alcohol dependence in RHS patients. Two brothers with the previous long-standing diagnosis of RHS and their mental symptoms of persecutory delusion and depression are reported, as well as the additional problem of alcohol dependence in one of them. The cerebellar dysfunction found in RHS may be associated with an underlying organic condition. Determination of the relationship between cerebellar dysfunction and psychosis in RHS will require further study. Although the mechanism of the suppression of myoclonus by alcohol remains unclear, patients should be allowed to drink socially, and alcohol consumption should not be totally prohibited. However, effective treatment of the problems of alcohol tolerance, abuse, or dependence requires the cooperation of both neurologists and psychiatrists.
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PMID:Progressive myoclonic epilepsies syndrome (Ramsay Hunt syndrome) with mental disorder: report of two cases. 1059 82

A 53-year-old woman who developed depression as the first symptom of multiple system atrophy was treated. Depression was followed successively by autonomic failure, parkinsonism and cerebellar ataxia. Treatment with L-DOPA, L-threo-DOPS, and thyroid releasing hormone was associated with improvement of autonomic failure and parkinsonism. As for depression, scores on the Zung scale and the Hamilton scale improved from 58 to 49 and from 30 to 22, respectively, This case is remarkable in that depression preceded neurologic dysfunction and was managed successfully by antiparkinsonian medication. A common underlying disturbance may be responsible for the depression and neurologic dysfunction in multiple system atrophy.
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PMID:Depression in multiple system atrophy: a case report. 1099 71


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