Gene/Protein Disease Symptom Drug Enzyme Compound
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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence of complications associated with disease and treatment was compared in younger versus elderly patients with Parkinson's disease (PD). One hundred sixty-five patient records were divided according to patient age into two groups ("younger," 41 to 64, and "elderly," > or = 65 years) and reviewed for the incidence of dyskinesias, fluctuations, freezing, psychosis, dementia, depression, and insomnia. Younger patients had a greater incidence of chorea (75.8 percent vs 49.5 percent), dystonia (82.3 percent vs 49.0 percent), fluctuations (90.1 percent vs 68.1 percent), depression (73.2 percent vs 36.8 percent), and insomnia (57.9 percent vs 18.1 percent). There were no significant differences in the incidence of freezing, dementia, or psychosis. At the time of the first adverse event, there was no difference in patient characteristics such as gender, lag time from disease diagnosis to levodopa initiation, disease symptoms at the time of diagnosis, levodopa dose, or concomitant drug use despite the fact that the older group had a longer duration of disease, higher Hoehn and Yahr stage, an older age at onset of PD, and longer duration of levodopa use. Younger patients with PD experience a greater incidence of adverse effects than do elderly PD patients. The spectrum of adverse effects is comparable to those of young-onset (< or = 40 years) patients.
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PMID:Complications of disease and therapy: a comparison of younger and older patients with Parkinson's disease. 887 56

Huntington's disease (HD) is a progressive neurodegenerative disorder affecting approximately 5-10 per 100,000 people in the UK (Harper, 1992). This dominantly inherited genetic condition causes movement disturbance (especially chorea), depression and dementia. The complex physical, mental, psychological and social problems caused by HD can result in particular difficulties in care. The course of the disease may span 15-20 years from diagnosis to death, necessitating long-term nursing care. The NHS and Community Care Act 1990 has made statutory provision for patients to be cared for at home if they so wish, placing a greater onus of care on the primary healthcare team. A survey of 25 patients in Somerset who had been diagnosed with HD was recently undertaken to ascertain the health and social care needs of patients and their carers. Of a possible 300 care needs in 12 categories (e.g. housing, dietary advice, carer support), 73 unmet needs were identified in this group. Using the survey as a basis, this article describes the steps taken in Somerset to ensure that the future needs of this group of patients are fulfilled. This model may be appropriate for the care of patients with other complex long-term diseases.
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PMID:Using research to develop care for patients with Huntington's disease. 911 44

Patients with Parkinson's disease (PD) are subject to a wide range of fluctuations in their clinical state, most of them treatment-related but some more disease-related. Short-duration motor fluctuations include freezing and paradoxic kinesis, lasting seconds to minutes. It is important to distinguish between "off" period freezing, which may be helped by measures to increase time "on," and freezing that is present in both "on" and "off" periods, which is difficult if not impossible to treat. Medium-duration fluctuations associated with chronic L-dopa treatment include wearing-off and "on-off" responses, which can involve (a) return of parkinsonism, (b) dyskinesias, and (c) non-motor fluctuations. A poorly understood long-duration pharmacodynamic response to L-dopa lasting up to 2 weeks may also be seen. This may manifest as late deterioration after L-dopa is withdrawn. More importantly, and more commonly, it is important to recognize that the ultimate effect of an alteration in L-dopa treatment may take 2 weeks to equilibrate in the brain. "Optimization" of L-dopa therapy is therefore not a realistic expectation during an inpatient admission and is instead primarily a long-term outpatient procedure. The "off" state is not the same as untreated PD, and may represent rebound worsening after the beneficial effect of L-dopa has worn off. Sometimes there is also transient worsening at the onset of effect of a dose. "Off' period dyskinesias tend to be relatively fixed, painful, and dystonic. Biphasic (beginning and/or end of dose) dyskinesias are often severe, ballistic, and stereotypic. Peak dose or "square wave" dyskinesias comprise a mix of mobile dystonia or chorea that is usually painless. Many patients experience any combination of panic, anxiety, and depression in their "off" periods, and many also experience pain, with instant relief as they turn "on." Other parameters that may vary between the "on" and "off" states include urinary and bowel dysfunction, blood pressure, respiratory function, and sweating attacks. Most but not all of these phenomena can be related to a simplistic but nevertheless usually practically useful model of differing levels of central dopaminergic stimulation. In difficult cases, an acute apomorphine challenge analogous to the effects of a "Tensilon test" in myasthenia gravis may help to determine whether a given clinical feature represents over- or understimulation of central dopamine receptors.
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PMID:Classification of fluctuations in patients with Parkinson's disease. 971 77

Thrombosis, thrombocytopenia, recurrent fetal loss and a variety of non-thrombotic neurological disorders have all been associated with antiphospholipid antibodies (aPL). Cerebral ischemia associated with aPL is the most common arterial thrombotic manifestation. Depression, cognitive dysfunction, depression and psychosis have all been associated with aPL. The presumed pathophysiologic mechanism underlying these manifestations is thought to be a result of cerebral ischemia in some, but not all cases. Seizures, chorea and transverse myelitis all appear to be associated with aPL. An interaction between aPL and central nervous system cellular elements rather than aPL-associated thrombosis seems to be a more plausible mechanism for these clinical manifestations. Migraine on the other hand, does not appear to be associated with aPL in either lupus or non-lupus populations. Neuroimaging studies show an increased frequency of brain abnormalities in patients with aPL, but none appear to be specific. The best treatment strategy for preventing neurological manifestations of aPL is not fully defined. For thrombotic manifestations, both antiplatelet and anticoagulant therapies have been suggested. In some patients, immunosuppressant therapy has been used. For non-thrombotic manifestations, some combination of immunosuppressant therapy and symptomatic treatment may be warranted.
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PMID:Neurological manifestations of antiphospholipid antibody syndrome. 981 77

Antiphospholipid antibodies (aPL) have been most strongly associated with a syndrome (APS) characterized by venous and/or arterial thrombosis, thrombocytopenia, recurrent fetal losses and a variety of non-thrombotic and thrombotic neurological disorders. Cerebral ischemia associated with aPL is the most common arterial thrombotic manifestation. Other neurological syndromes, such as cognitive dysfunction, dementia, psychosis, depression, seizures, chorea and transverse myelopathy, have all been associated with antiphospholipid antibodies.
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PMID:Neurological involvement in antiphospholipid antibodies syndrome (APS). 1107 18

There is nothing more discouraging than for a patient to be given a specific diagnosis, then to be told that there is nothing that can be done. Physicians are equally disheartened to see exponential progress being made in the understanding of the pathophysiology of a complex disorder but few direct benefits resulting for their patients. Over the past 5 years, molecular genetic research has completely revolutionized the way in which the progressive cerebellar ataxias are classified and diagnosed, but it has yet to produce effective gene-based, neuroprotective, or neurorestorative therapies. The treatment of cerebellar ataxia remains primarily a neurorehabilitation challenge, employing physical, occupational, speech, and swallowing therapy; adaptive equipment; driver safety training; and nutritional counseling. Modest additional gains are seen with the use of medications that can improve imbalance, incoordination, or dysarthria (amantadine, buspirone, acetazolamide); cerebellar tremor (clonazepam, propranolol); and cerebellar or central vestibular nystagmus (gabapentin, baclofen, clonazepam). Many of the progressive cerebellar syndromes have associated features involving other neurologic systems (eg, spasticity, dystonia or rigidity, resting or rubral tremor, chorea, motor unit weakness or fatigue, autonomic dysfunction, peripheral or posterior column sensory loss, neuropathic pain or cramping, double vision, vision and hearing loss, dementia, and bowel, bladder, and sexual dysfunction), which can impede the treatment of the ataxic symptoms or can worsen with the use of certain drugs. Treatment of the associated features themselves may in turn worsen the ataxia either directly (as side effects of medication) or indirectly (eg, relaxation of lower limb spasticity that was acting as a stabilizer for an ataxic gait). Secondary complications of progressive ataxia can include deconditioning or immobility, weight loss or gain, skin breakdown, recurrent pulmonary and urinary tract infections, aspiration, occult respiratory failure, and obstructive sleep apnea, all of which can be life threatening. Depression in the patient and family members is common. Although no cures exist for most of the causes of cerebellar ataxia and there are as yet no proven ways to protect neurons from premature cell death or to restore neuronal populations that have been lost, symptomatic treatment can greatly improve the quality of life of these patients and prevent complications that could hasten death. Supportive interventions should always be offered-- education about the disease itself, genetic counseling, individual and family counseling, referral to support groups and advocacy groups, and guidance to online resources. Misinformation, fear, depression, hopelessness, isolation, and financial and interpersonal stress can often cause more harm to the patient and caregiver than the ataxia itself.
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PMID:Cerebellar Ataxia. 1109 49

The treatment of patients with neuropsychiatric systemic lupus erythematosus (NPSLE) can be difficult and complex owing to the variety of nervous system manifestations that can occur, which include peripheral nerve disease, headaches, seizures, cerebrovascular disease, chorea, transverse myelitis, and psychiatric and cognitive disorders. Many of these manifestations can result from metabolic abnormalities or infection or as side effects of medications. Thus, in any patient with suspected NPSLE, it is crucial to exclude secondary causes of the presenting symptoms before assuming that they are due to NPSLE. It is especially important to exclude infection because this is a common cause of both morbidity and mortality in patients with systemic lupus erythematosus (SLE). Symptoms such as anxiety and depression may or may not be related to disease activity. Treatment decisions are based on accurate diagnosis of the specific NPSLE manifestation, which is usually made using tools such as brain imaging, electroencephalography, cerebrospinal fluid analysis, nerve conduction studies, or special serologic tests (eg, determination of antiphospholipid or antiribosomal P antibody levels). It is also important to assess the degree of other SLE- mediated systemic disease activity in a patient with neurologic manifestations to determine if activation of systemic disease activity is also occurring. This is done by measuring complement levels, anti-double-stranded DNA levels, complete blood count, and urinalysis. For some NPSLE manifestations (eg, infrequent seizures, headaches, depression, anxiety, or peripheral neuropathy) that appear without activation of systemic disease, symptomatic treatment is appropriate. For others (eg, psychosis, delirium, or transverse myelopathy without other obvious cause), treatment with high-dose glucocorticoids with or without cyclophosphamide is appropriate whether there is evidence of other systemic disease activity or not. In general, the activity and severity of the leading organ manifestations dictate pharmacologic treatment.
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PMID:Neuropsychiatric Systemic Lupus Erythematosus. 1109 72

McLeod syndrome is a distinct form of neuroacanthocytosis. Its defining feature is the depression of erythrocyte Kell antigens. The underlying X chromosomal mutations cause a dysfunction of an erythrocyte membrane protein Kx. A choreatic movement disorder with caudate atrophy in CT and MRI has been reported in McLeod syndrome later in the course of the disease. Positron emission tomography with 18F-deoxyglucose (FDG) was performed in two unrelated affected men. In the older patient, progressive chorea was seen from the 5th decade. In the second patient there were no signs of a movement disorder at the age of 28. Positron emission tomography disclosed a reduction of the striatal FDG uptake in both patients, with accentuation in patient 1. Frontal lobe metabolism was not affected. Basal ganglia dysfunction with early impairment of striatal glucose metabolism thus seems obligatory for McLeod syndrome, as found in other forms of chorea with or without acanthocytosis.
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PMID:Reduction of striatal glucose metabolism in McLeod choreoacanthocytosis. 1125 78

The McLeod syndrome is an X-linked disorder caused by mutations of the XK gene encoding the XK protein. The syndrome is characterized by absent Kx erythrocyte antigen, weak expression of Kell blood group system antigens, and acanthocytosis. In some allelic variants, elevated creatine kinase, myopathy, neurogenic muscle atrophy, and progressive chorea are found. We describe a family with a novel point mutation in the XK gene consisting of a C to T base transition at nucleotide position 977, introducing a stop codon. Among seven affected males, five manifested with psychiatric disorders such as depression, bipolar disorder, or personality disorder, but only two presented with chorea Positron emission tomography and magnetic resonance volumetry revealed reduced striatal 2-fluoro-2-deoxy-glucose (FDG) uptake and diminished volumes of the caudate nucleus and putamen that correlated with disease duration. In contrast, none of 12 female mutation carriers showed psychiatric or movement disorders. However, a semidominant effect of the mutation was suggested by erythrocyte and blood group mosaicism and reduced striatal FDG uptake without structural abnormalities. Therefore, patients with psychiatric signs or symptoms segregating in an X-linked trait should be examined for acanthocytosis and Kell/Kx blood group serology.
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PMID:McLeod syndrome: a novel mutation, predominant psychiatric manifestations, and distinct striatal imaging findings. 1126 14

Voluntary motor impairment is a functionally important aspect of Huntington's disease (HD). Therefore, quantitative assessment of disturbed voluntary movement might be important in follow-up. We investigated the relation between quantitatively assessed daytime motor activity and symptom severity in HD and evaluated whether assessment of daytime motor activity is a responsive measure in the follow-up of patients. Sixty-four consecutive HD patients and 67 age- and sex-matched healthy controls were studied. Daytime motor activity was recorded using a wrist-worn activity monitor that counts all movements during a period of five consecutive days. Patients were rated clinically for voluntary motor impairment, dyskinesias, posture & gait, depression, cognitive impairment and functional capacity. Follow-up was available from 40 patients (mean follow-up 2.0 years) and 29 controls (mean follow-up 5.9 years). Despite chorea, patients had less daytime motor activity than controls (P < 0.005). This hypokinesia correlated with impaired voluntary movements (r = 0.37; P < 0.01), disturbed posture & gait (r = 0.38; P < 0.005) and especially with reduced functional capacity (r = 0.51; P < 0.0005). During follow-up, hypokinesia remained unchanged in clinically stable patients, but became worse in those whose functional disability progressed (P < 0.005). Hypokinesia seems a core symptom of HD which is related to functional capacity. Actimetric assessment of hypokinesia is responsive to disease progression and can be used as an objective tool for follow-up.
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PMID:Quantitative assessment of daytime motor activity provides a responsive measure of functional decline in patients with Huntington's disease. 1139 42


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