Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Despite astounding progress in the biochemical management of Parkinson's disease in particular and of other movement disorders, there are still patients disabled by severe tremor and not by bradykinesia in whom thalamotomy remains the treatment of choice. Though the irreducible complications of surgery must be taken into account, the problems of prolonged multiple drug therapy should not be ignored. The same rationale applies to selected patients with essential or familial tremor. For some patients with ataxic tremor caused by multiple sclerosis and other brain lesions, or with dystonia or, rarely, other movement disorders, thalamotomy may offer limited though significant relief from an otherwise intractable disability. Indications for the use of stereotactic destructive lesions in the treatment of nociceptive pain in those cases where cordotomy and intraspinal morphine infusion are unsuitable have contracted with the introduction of lower-risk alternatives such as intraventricular morphine instillation. When destructive lesions are indicated, the choice will lie between mesencephalic tractotomy, with its higher success rate but irreducible mortality and morbidity, and medial thalamotomy, which, though less risky, is also less effective. For central and deafferentation pain, the same two procedures may be considered. However, destructive lesions are seldom effective for the treatment of the most common element of these pain syndromes: steady burning or dysesthetic pain. They may be more promising, though, for the intermittent, often shooting pain and the evoked elements (hyperpathia and allodynia) of central and deafferentation pain. Even so, it is advisable first to carry out a trial of VC and PVG stimulation before considering a destructive lesion, which should be a last resort.
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PMID:Thalamotomy. 213 73

In an open pilot study, 10 patients with Parkinson's disease and nocturnal and/or early-morning disabilities were given Madopar HBS (hydrodynamically balanced system; mean dose 250 mg) shortly before retiring in addition to their usual daytime antiparkinsonian treatment. Eight patients derived worthwhile improvement; the most gratifying responses were seen in the relief of nocturnal bradykinesia, rigidity and tremor. Early-morning symptoms were also improved in 3 out of 5 patients, possibly as a secondary response to an improved nights sleep. Cramps, early-morning dystonia and pain, however, responded poorly. Overall results are sufficiently encouraging to warrant further controlled studies with Madopar HBS in what has been a relatively neglected area of distress for many patients with Parkinson's disease.
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PMID:A sustained-release formulation of L-dopa (Madopar HBS) in the treatment of nocturnal and early-morning disabilities in Parkinson's disease. 342 6

We report a right-handed 62-year-old man with early onset familial parkinsonism. The patient was well until 24 years of the age when he noted an onset of resting tremor in his right hand. During the next four years, he noted rigidity, bradykinesia, and difficulty in walking. He was seen in another hospital at 28 years of the age, where he received left pallidotomy. Rigidity on the left side showed marked improvement. He received right pallidotomy at age 30 years. He developed right hemiplegia after this surgery. He was admitted to our hospital in March, 1983 when he was 51 years of the age. He was treated with levodopa but improvement was rather of minor degree. He was transferred to another hospital, but his motor disturbance progressed slowly, and was admitted again to our hospital in November 1990. He had 6 siblings 4 of whom including himself suffered from parkinsonism. No consanguinity was noted in parents. On admission, he appeared chronically ill but the general physical examination was unremarkable. Neurologic examination revealed an alert and mentally sound man. Hasegawa dementia scale was 28.5/32.5. Upward gaze was slightly restricted (3/5). Cranial nerve examination revealed oculogyric crisis, apraxia of eyelid opening, masked face, and small voice. He was able to stand with support; his posture showed left-ward leaning. He had right hemiparesis with moderate weakness. He showed marked bradykinesia and moderate rigidity in his left upper extremity. Fine postural tremor was noted in the left hand. Deep tendon reflexes were diminished in the upper extremities. No Babinski sign was noted. Pain sensation was somewhat diminished on the right side. Results of routine laboratory examination were unremarkable. Cranial CT scan revealed atrophy in the frontal lobe, particularly in the prefrontal area. In addition, MRI revealed T1-and-T2-low signal intensity lesions in the right ventral pallidal region and in the left ventrolateral thalamic-hypothalamic areas. He was treated with 600 mg of levodopa with benserazide and 22.5 mg of bromocriptine with mild to moderate improvement in his bradykinesia and rigidity. He was discharged in January 1991. His clinical course was complicated by intestinal obstruction in October, 1994. He was admitted to another hospital where he was operated on the obstruction on November 5, 1994. The sigmoid colon was markedly dilated but no mass was found. Postoperative course was uneventful until November 18, 1994 when he was found dead in his hospital room shortly after 4 am. The patient was discussed in neurological CPC, and the chief discussant arrived at the conclusion that the patient had young-onset familial Lewy body-negative parkinsonism. Opinions were divided between Lewy body-positive familial Parkinson's disease and Lewy body negative young onset parkinsonism. Postmortem examination revealed aspiration pneumonia, which appeared to be the cause of his death, in the right lung. Neuropathologic examination revealed loss of malanized neurons in the substantia nigra and the locus coeruleus. In the substantia nigra, neuronal loss was particularly severe in the ventrolateral area. No Lewy bodies were seen. The dorsal motor nucleus of the vagal nerve was well preserved. Stereotaxic lesions involved bilateral thalamic areas. This patient appears to represent a case of autosomal recessive juvenile parkinsonism (AR-JP). Early onset, superb response to levodopa, sleep effect, and easy development of dyskinesias and motor fluctuations characterize AR-JP. The reason why this patient did not show these clinical features is probably bilateral sterotaxic surgeries. Particularly, the second surgery was complicated by right hemiparesis. His siblings who developed parkinsonism showed typical clinical features of AR-JP.
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PMID:[A 62-year-old man with familial parkinsonism with the onset at 24 years of the age]. 870 64

Delirium is common among cancer patients, especially those with advanced disease. Typical treatment involves addressing the underlying cause if possible; eliminating nonessential and/or other drugs that can worsen confusion, manipulating the environment; and administering antipsychotic drugs to control symptoms and agitated behavior, and attempt to clear the patient's sensorium. The newer atypical antipsychotics may have potential in the treatment of delirium and also have the added benefit of causing less akithisia and other extrapyramidal side effects. This is illustrated by the case of a 59-year-old woman with leukemia and pain of unclear etiology who developed a delirium and a moderate to severe extrapyramidal syndrome (EPS) in the setting of escalation of her pain medications and concomitant escalation of prochlorperazine. The patient presented with confusion and moderate to severe cogwheeling rigidity, masked facies, bradykinesia, and tremor. Additionally, the patient had a relatively recent history of subdural hematoma and one seizure. Conservative management including eliminating multiple nonessential medications (including the prochlorperazine); changing her opioid analgesic; providing a 24-hour companion: and administering low doses of haloperidol (0.5 mg-2.0 mg) were not effective in treating the patient's delirium. The patient's EPS was dramatically worse following haloperidol doses. After approximately I week without improvement, the patient was started on olanzapine 5 mg daily with initial improvement but with residual confusion in the evenings and overnight. The dose was titrated up to 10 mg nightly with 2.5 mg as needed during the day. After 3 days on this regimen, the patient's mental status exam was normal and she was discharged home. We discuss the potential utility of this atypical antipsychotic in the palliative care setting.
J Pain Symptom Manage 1999 Mar
PMID:Complicated delirium in a cancer patient successfully treated with olanzapine. 1009 65

Parkinson's disease (PD) is a chronic progressive neurological disorder characterized by tremor, muscle rigidity, slowness of movement (bradykinesia), and gait instability. In early disease, PD is well managed in an office setting, however, as the disease progresses, a variety of syndromes may result in emergency department visits. The scenarios most likely to require an emergent evaluation are severe motor "off" periods with immobility, involuntary movements (dyskinesia), psychosis, acute confusion, panic disorder, and pain. Other less frequent presentations are also discussed. This article uses illustrative cases to provide a framework to discuss emergency department diagnosis and management issues in caring for these patients.
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PMID:Emergency department presentations of patients with Parkinson's disease. 1075 Sep 35

Parkinson's disease is one of the most frequent neurodegenerative diseases. The usual characteristic signs combine the classical triad, rest tremor, bradykinesia and rigidity. The diagnosis is usually easy after several years, especially when the levodopa responsiveness is established, and most of the differential diagnosis can then be ruled out. However, the diagnosis of Parkinson's disease is not confirmed at autopsy in 25% of cases. The errors are much more frequent at disease onset since the clinical presentation may be insidious and may comprise non-motor signs such as pain, vegetative, sensory or neuropsychological signs. In the future, early recognition of the disease will become more and more important with the development of neuroprotective therapeutic strategies.
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PMID:[Circumstances of Parkinson's disease diagnosis]. 1596 14

Despite the current efficacious symptomatic approaches, the search is on for new therapies for Parkinson's disease that can control the cardinal symptoms of the disease (tremor, rigidity and bradykinesia), control/prevent motor complications induced by long-term levodopa, act on non-motor disease symptoms (dementia, dysautonomia, pain, insomnia, falls) and halt disease progression. Rasagiline is a monoamine oxidase-B inhibitor that has demonstrated efficacy against the cardinal symptoms of Parkinson's disease when used as monotherapy in early Parkinson's disease, and as an adjunct to levodopa in advanced disease stages. It reduces the duration and severity of poor symptom response episodes in fluctuating patients. Preliminary results allow discussion of putative effects of rasagiline on some non-motor signs and disease progression. This article outlines the evidence surrounding the efficacy and safety of rasagiline, and discusses its potential to address some of the currently unmet needs of Parkinson's disease therapy.
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PMID:Rasagiline in the pharmacotherapy of Parkinson's disease--a review. 1619 59

Parkinsonism is a clinical syndrome characterized by bradykinesia, hypo-/ akinesia, muscular rigidity, and resting tremor, mainly caused by Parkinson's disease (PD). Progressive loss of nigral neurons with Lewy bodies is considered an essential neuropathological feature. Recent studies, however, indicate that nigral degeneration is only a part of this synucleinopathy, and clinical symptoms go far beyond motor parkinsonism. Olfactory disturbances, autonomic dysfunction, pain, sleep fragmentation, depression, and dementia with or without psychosis are frequently seen. The variability in the expression of these signs and symptoms suggests multiple causes and/or pathogeneses within the present diagnostic disease entity. In this article, a recently proposed staging of PD-related brain pathology will be correlated with the various clinical expressions. It will be argued that the specific topographical sequence of the pathology, depending on the extent and progression of the degenerative process at defined sites, may explain the individually variable expression of this disease.
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PMID:Parkinson's disease: premotor clinico-pathological correlations. 1701 46

This study examined the frequency and degree of caregiver burden in persons with parkinsonism, a group of disorders with four primary symptoms that include tremor, rigidity, postural instability, and bradykinesia. We assessed associations between perceived caregiver burden and physical, cognitive, and functional impairments using well-established tools for persons with parkinsonism. The 49 individuals with parkinsonism ranged in age from 61 to 87 (mean = 75), while their caregivers (N = 49) ranged in age from 48 to 83 (mean = 70). The caregivers were predominantly either wives (82%) or daughters (6%), with other family members, friends, and/or neighbors (12%) making up the rest. The caregivers reported a relatively high ability for coping (mean scores = 4.6/6). Caregiver burden was significantly negatively associated with activities of daily living and motoric difficulties as measured on the Unified Parkinson's Disease Rating Scale (UPDRS). Likewise, caregiver burden was negatively associated with caregiver self-reported sleep and coping ability. Results did not demonstrate an association on the UPDRS among mentation, behavior, and mood. We found a significant negative correlation for mentation between the Folstein Mini-Mental Status Examination and caregiver burden measures; however, we did not find this association with the Dementia Rating Scale-2. Patient's self-reported pain and caregiver burden were not associated.
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PMID:Caregiver distress in parkinsonism. 1712 89

Parkinson's disease (PD) is characterized by resting tremor, rigidity and bradykinesia. In 80% of cases, the disorder begins with upper limb resting tremor. However, there are some presenting atypical features that make the diagnosis even more difficult and intriguing. The disorder can have its onset below 40 years old, characterizing early-onset parkinsonism, which differential diagnosis possibilities are varied. Atypical presentations include a pure akinetic-rigid syndrome, the initial manifestations occurring in the lower limbs, and pain as the most important or sole manifestation. These atypical features are unusual, but can be seen in clinical practice. We present a 37 years old woman with early-onset parkinsonism beginning with an akinetic-rigid syndrome in the lower limbs whose first symptom was left leg pain, which diagnosis was made after 4 years of onset and after 16 referrals to several experts in different fields. We discuss these atypical features and the diagnostic pitfalls in PD.
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PMID:Diagnostic pitfalls in Parkinson's disease: case report. 1760 43


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