Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027066 (myoclonus)
 4,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study objective was to determine whether switching patients from morphine to transdermal fentanyl resulted in a reduction of morphine-associated side effects, and an improvement in cognitive function and patients' well being while maintaining adequate pain and symptom control. Nineteen patients aged 42-86 with terminal cancer, maintained on morphine for pain and distressed as a result of morphine toxicity, were given the dose of fentanyl corresponding to their current morphine dose. Pain control was then maintained (mostly fentanyl 50-100 microg/h) over the 14-day study period. Throughout the study, patients' global assessment of well being (primary efficacy variable) was statistically significantly improved. Sleepiness and drowsiness were significantly less of a problem. There was a trend towards improvement in attention span/concentration, and in the power and quality of concentration. Cognitive function tests also revealed a significant improvement in working (short term) and speed of memory although not in secondary (long term) memory. Patients did not experience hallucinations or delusions and there was no change in levels of anxiety or depression (Hospital Anxiety Depression Scale). The incidence of dizziness was significantly reduced, and there was a nonsignificant decrease in number of patients who suffered myoclonus and in the severity of this condition over the 14 days. The investigator's overall impression of treatment with transdermal fentanyl was 'fair', which was not in agreement with the positive impression expressed by patients (score 74, range: 0 worst, 100 best). Further work is required to determine if the improvement in patients' well being and cognitive function is achieved in larger study populations.
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PMID:Opioid switching from morphine to transdermal fentanyl for toxicity reduction in palliative care. 1238 Jun 61

An old antimalarial drug quinacrine is one of the compounds that can inhibit the accumulation of pathogenic prion protein in cultured neuroblastoma cells. Here we report the result of a clinical trial of quinacrine administration to a patient with Creutzfeldt-Jakob disease (CJD). A 37-year-old woman was admitted to our hospital for ataxic gait, hallucination and dementia in August 2001. As a past history she had received an operation for cerebellar astrocytoma and had a cadaveric dura mater graft at 14 years old. After hospitalization she showed signs of anxiety, stimulus-sensitive myoclonus, decorticate rigidity, then deteriorated pursuit eye movement and voluntary limb movement. The ethics committee of Dokkyo University hospital approved this treatment, and the family of the subject was fully informed as to the nature and purpose of the treatment and gave their consent. One week after the administration of 300 mg/day of quinacrine, voluntary limb movement and pursuit eye movement appeared. There was PSD on EEG, but one week after administration of the quinacrine, PSD disappeared, and a theta wave was recognized as the basic activity on the EEG. But her symptoms deteriorated again after 3 weeks, and PSD appeared. Liver dysfunction developed 2 months after administration, and the administration of quinacrine had to be stopped. Quinacrine was administrated to a CJD patient who received a cadaveric dura mater graft and developed CJD 23 years later. The symptoms of the patient were transiently improved with the disappearance of PSD on EEG. Although the mechanism of quinacrine for the central nervous system is still unclear, this case suggests that quinacrine may be clinically one possible drug for treating CJD.
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PMID:[Quinacrine administration to a patient with Creutzfeldt-Jakob disease who received a cadaveric dura mater graft--an EEG evaluation]. 1458 66

Pellagra is caused by nicotinic acid deficiency; it is rarely encountered in developed countries, and it is mainly related to poverty and malnutrition, as well as with chronic alcoholism. We report the case of an alcoholic patient who was diagnosed with pellagra and administered B-complex vitamin tablets that did not contain niacin. A few weeks later, the patient developed nervousness, irritability, insomnia and, consequently, delusional ideas and hallucinations, for which he had to be hospitalized. After his admission, the patient manifested loss of consciousness and myoclonus. All of his symptoms (cutaneous, neurological, and psychiatric) resolved fully with treatment with niacin in combination with other B-complex vitamins. All undiagnosed encephalopathies in alcoholic patients should be treated with multiple vitamin therapy, including nicotinic acid.
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PMID:Pellagra encephalopathy following B-complex vitamin treatment without niacin. 1524 45

We report a patient with subacute diffuse encephalopathy characterised by rapidly progressive dementia with visual hallucinations, myoclonus and generalised seizures. She was euthyroid but showed high serum levels of thyreoglobulin and thyreoperoxidase antibodies. Hashimoto's encephalopathy was diagnosed. MRI of the brain in the acute phase demonstrated no structural abnormalities. However in the mesotemporal regions and the anterior parts of the brain, a decrease of the N-acetylaspartate and an increase of the Choline-containing compounds was found on MRI-spectroscopy. Reversal of these abnormalities was demonstrated a few months later after starting therapy. Plasmapheresis resulted in normalisation of serum levels of the antibodies and rapid clinical improvement. This observation supports the idea that a correlation exists between the serum levels of the thyroid auto-antibodies and the course of the clinical illness.
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PMID:Subacute Hashimoto's encephalopathy, treated with plasmapheresis. 1550 71

Parkinson's disease is associated with classical Parkinsonian features that respond to dopaminergic therapy. Neuropsychiatric sequelae include dementia, major depression, dysthymia, anxiety disorders, sleep disorders, and sexual disorders. Panic attacks are particularly common. With treatment, visual hallucinations, paranoid delusions, mania, or delirium may evolve. Psychosis is a key factor in nursing home placement, and depression is the most significant predictor of quality of life. Clozapine may be the safest treatment for psychotic features, but more research is needed to establish the efficacy of antidepressant treatments. Dementia with Lewy bodies, the second most common dementia in the elderly, may present in association with systematized delusions, depression, or RBD. Early evidence suggests the utility of rivastigmine, donepezil, low-dose olanzapine, and quetiapine in treating DLB. Parkinson-plus syndromes generally lack a good response to dopaminergic treatment and evidence additional features, including dysautonomia, cerebellar and pontine features, eye signs, and other movement disorders. MSA is associated with dysautonomia and RBD. SND (MSA-P) is associated with frontal cognitive impairments, but dementia, psychosis, and mood disorders have not been strikingly apparent unless additional pathological findings are present. In SDS (MSA-A), impotence is almost ubiquitous; urinary incontinence is frequent; depression is occasional, and sleep apnea should be treated to avoid sudden death during sleep. OPCA neuropsychiatric correlates await further definition. Progressive supranuclear palsy neuropsychiatric features include apathy, subcortical dementia, pathological emotionality, mild depression and anxiety, and lack of appreciable response to donepezil. CBD usually is recognized by early frontal dementia with ideomotor apraxia, often in the right upper extremity, attended later by poorly responsive unilateral Parkinsonism, with additional signs including cortical reflex myoclonus, limb dystonia, alien limb, oculomotor apraxia when asked to look horizontally, depression, personality changes, and, occasionally, Kluver-Bucy syndrome. The neuropsychiatry of FTDP-17 involves apraxia, executive impairment, personality changes, hyperorality, and occasional psychosis. Future research in these Parkinsonian disorders should target the characterization of neuropsychiatric sequelae and their treatment.
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PMID:The neuropsychiatry of Parkinson's disease and related disorders. 1555 Feb 93

Kufor Rakeb disease is an autosomal recessive disorder characterized by subacute, juvenile-onset, levodopa-responsive parkinsonism, pyramidal signs, dementia, and a supranuclear gaze palsy. It was originally described more than a decade ago, and linkage analysis identified a locus on chromosome 1p36 that was previously assigned PARK9. We have further characterized the clinical picture and specifically re-assessed the response to levodopa in the original family, in the northern highlands of Jordan. In the 4 surviving patients, there has been a narrowing of the therapeutic window for levodopa with the emergence of peak-dose dyskinesias with increased spasticity and cognitive decline. Several new features were identified, including facial-faucial-finger mini-myoclonus, visual hallucinations, and oculogyric dystonic spasms.
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PMID:Kufor Rakeb disease: autosomal recessive, levodopa-responsive parkinsonism with pyramidal degeneration, supranuclear gaze palsy, and dementia. 1598 21

Visual-spatial agnosis, praxis deficits and hallucinations can be the features of subacute sclerosing panencephalitis (SSPE) in the early period. This study describes a 15-year-old boy with SSPE presenting with visual agnosia, prosopagnosia, simultanagnosia, optic ataxia, and oculomotor apraxia which are compatible with Balint syndrome. MRI revealed heterogenous and abnormal signal changes in the bilateral parieto-occipital areas. The signals were more prominent on the left. The case discussed herein is important because he was diagnosed as Balint's syndrome by means of clinical and neuroradiological findings before the onset of known symptomatology as dementia/myoclonus of SSPE. The case is also illustrative of the need to emphasize the prompt evaluation of a patient's cortical features before clinical progression becomes apparent. This evaluation should be performed in the early period if correct diagnosis is to be reached.
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PMID:Subacute sclerosing panencephalitis presenting with Balint's syndrome. 1637 13

Pain is not the most frequent symptom in cancer patients, but it is considered the most serious and threatening symptom. Opioid analgesics are the mainstay for analgesic treatment of cancer patients. Methadone is increasingly being considered as an alternative to morphine and seems to become relatively more potent with increasing exposure to other opioids. "Newer" side effects of opioids have been demonstrated, including cognitive impairment, generalized allodynia/hyperalgesia, myoclonus and hallucinations. When the pain relief effects of oral opioids have been exhausted, other pain management approaches, including spinal delivery of analgesics, may be effective alternatives.
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PMID:[Cancer-related pain]. 1676 93

Opioids, defined as drugs that stimulate opioid receptors, are primarily used in the treatment of moderate to severe pain. They induce central nervous system (CNS) adverse effects which can be divided into three groups. The first group includes effects that lower the level of consciousness-sedation, drowsiness and sleep disturbance. The second group affects the thinking process and the ability to react-cognitive impairment, psychomotor impairment, delirium, hallucinations, dreams and nightmares. The third group is of the direct toxic effects of opioids on neurons and includes myoclonus (perhaps), hyperalgesia and tolerance. This review addresses the incidence, possible mechanisms, and treatment of each of these groups of opioid-induced adverse effects.
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PMID:Adverse effects of opioids on the central nervous systems of palliative care patients. 1743 Aug 25

A 50-year-old woman who was being treated with hemodialysis was admitted for severe neuropsychiatric symptoms. She tested positive for antibody to hepatitis C virus. Her medical history revealed ophthalmic herpes zoster four days before her admission for which she was started on oral acyclovir (800 mg three times daily). Four days later, she became disoriented and agitated. She had visual hallucinations and myoclonus. She was diagnosed as having acyclovir toxicity and was instituted on vigorous dialysis. The serum acyclovir levels normalized and the patient became asymptomatic with three dialysis sessions. Our case further reinforces that the dose of acyclovir should be reduced in patients with renal failure and that dialysis is a good form of treatment for over dosage.
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PMID:Neuropsychiatric manifestations in a patient undergoing hemodialysis caused by treatment with oral acyclovir. 1820 66


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