Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085632 (apathy)
 4,089 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Differences in the expression of non-motor symptoms (NMS) by Parkinson's disease (PD) patients may have important implications for their management and prognosis. Gender is a basic epidemiological variable that could influence such expression. The present study evaluated the prevalence and severity of NMS by gender in an international sample of 951 PD patients, 62.63% males, using the non-motor symptoms scale (NMSS). Assessments for motor impairment and complications, global severity, and health state were also applied. All disease stages were included. No significant gender differences were found for demographic and clinical characteristics. For the entire sample, the most prevalent symptoms were Nocturia (64.88%) and Fatigue (62.78%) and the most prevalent affected domains were Sleep/Fatigue (84.02%) and Miscellaneous (82.44%). Fatigue, feelings of nervousness, feelings of sadness, constipation, restless legs, and pain were more common and severe in women. On the contrary, daytime sleepiness, dribbling saliva, interest in sex, and problems having sex were more prevalent and severe in men. Regarding the NMSS domains, Mood/Apathy and Miscellaneous problems (pain, loss of taste or smell, weight change, and excessive sweating) were predominantly affected in women and Sexual dysfunction in men. No other significant differences by gender were observed. To conclude, in this study significant differences between men and women in prevalence and severity of fatigue, mood, sexual and digestive problems, pain, restless legs, and daytime sleepiness were found. Gender-related patterns of NMS involvement may be relevant for clinical trials in PD.
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PMID:Gender-related differences in the burden of non-motor symptoms in Parkinson's disease. 2223 22

Parkinson's disease (PD) affects about 1 % of the population over the age of 60 years and is characterized by a combination of rest tremor, bradykinesia, rigidity, postural instability, stooped posture and freezing of gait (FoG). However, the clinical spectrum also spans a wide range of non-motor symptoms, such as depression, apathy, cognitive disorders, sleepiness, fatigue and pain. Given that the loss of dopamine in the striatum is the primary pathochemical hallmark in PD, pharmacological treatment of the disease has focused on restoring dopaminergic neurotransmission. The currently licensed dopaminergic treatments for PD modulate all the key steps in the dopamine transmission except the most powerful determinant of extracellular dopamine concentrations: the presynaptic dopamine transporter (DaT). Methylphenidate is a CNS stimulant that blocks the DaT and the noradrenaline (norepinephrine) transporter in the striatum and the prefrontal cortex in particular. Here, we report on and discuss the main open-label studies and randomized controlled trials on the effect of methylphenidate on severe gait disorders (e.g. the FoG) and non-motor symptoms in advanced PD. The various pharmacodynamic effects of methylphenidate mean that the drug may have significant value in the treatment of PD. However, there is a lack of randomized controlled trials in this field. Furthermore, more rigorous selection of the types and doses of the associated dopaminergic treatments is required because these parameters may profoundly influence the mechanisms of action of methylphenidate and the clinical outcomes. Pharmacogenetic tools could be of use in better defining study patients as a function of their dopaminergic metabolism and drug responsiveness.
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PMID:Methylphenidate : a treatment for Parkinson's disease? 2316 Sep 37

Parkinson's disease (PD) is traditionally viewed as a motor disorder with a characteristic triad of tremor, rigidity and bradykinesia. There is now increasing awareness that PD is a complex systemic disorder with many nonmotor symptoms (NMS) which include autonomic dysfunction, sleep disorders, sensory and neuropsychiatric features. NMS become more common in severity and frequency with advancing disease when neuropsychiatric features such as cognitive impairment and psychosis dominate the clinical picture. NMS are strongly correlated with quality of life for patients and their families as well as institutional care placement. Despite their importance, NMS are poorly recognized by clinicians and often undeclared by patients. Use of a validated screening tool NMSQuest followed by specific symptom assessment instruments strengthens the recognition and holistic management of NMS in PD. Some NMS such as mood disturbance, anxiety, pain and insomnia may be improved by optimization of dopaminergic therapy. Conversely, psychosis, excess daytime somnolence or impulse control disorder (ICD) may be triggered by dopaminergic drugs. Other NMS such as dementia and severe depression may be unresponsive to dopaminergic treatment and may reflect perturbations in cholinergic, serotonergic or noradrenergic neurotransmitter function. These symptoms are more challenging to manage but may be ameliorated to some extent by agents such as acetylcholinesterase inhibitor or antidepressant drugs. This contribution reviews the evidence for the evaluation and management of key NMS in PD (apathy, anxiety, depression, psychosis, dementia, ICD, sleep disturbance, autonomic dysfunction, pain) and highlights the urgent need for both novel therapies and more controlled trials for current therapeutic strategies.
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PMID:Evaluation and management of the non-motor features of Parkinson's disease. 2325 43

Neurobehavioral changes observed in patients with brain tumours may appear as cognitive deficits, mood disturbances, changes in behaviour or decreased adaptability (e.g., drowsiness, apathy, loss of spontaneity, fatigue). They are initially subtle, develop insidiously, and their severity often changes. Serious diagnostic problems can be caused by mood disorders, psychotic symptoms, personality changes, from disinhibition to apathy, observed in such patients. The problem in distinguishing them from organic psychiatric disorders, often poses a challenge for psychiatrists, neurologists and general practitioners. We describe a case difficult to diagnose because of apathy, due to a brain tumour in the right frontal lobe, diagnosed as depression. Another difficulty, rather suggesting mood disorder, was rheumatoid arthritis. Thorough and meticulous analysis of clinical data, neuropsychological assessment and neuroimaging diagnosis may help to assess aetiology of the observed disorders which can have similar clinical pictures but various causes.
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PMID:[Depression or apathy? A diagnostic trap: a huge right frontal lobe meningioma diagnosed and treated as mild atypical depression episode--a case study]. 2339 28

Myotonic dystrophy type 1 (DM1) represents the 1 chronic neuromuscular disease with the most prominent sleep disorders, including excessive daytime sleepiness (EDS), sleep apneas, periodic leg movements during sleep, and rapid eye movement sleep dysregulation. The large majority of DM1 patients complain about EDS, which may have a deleterious impact on work, domestic responsibilities, social life, and quality of life. Here, we review the extant literature and report that studies are largely supportive of the view that DM1-related EDS is primarily caused by a central dysfunction of sleep regulation rather than by sleep-related disordered breathing (SRDB) or sleep fragmentation. The pathogenesis of EDS in DM1 still remains unclear but several arguments favor a model in which brain/brainstem nuclear accumulations of toxic expanded DM protein kinase (DMPK) gene are responsible for aberrant genes expression in modifying alternative splicing. Regarding management, early recognition, and treatment of SRDB with nocturnal noninvasive mechanical ventilation is first mandatory. However, despite its appropriate management, EDS often persists and may require a psychostimulant but no consensus has been yet established. Further studies are needed to clarify the discrepancies between daytime sleepiness/fatigue complaints and subjective/objective measurement of daytime sleepiness, the role of cognitive impairment and apathy in this relationship, and its reversibility with appropriate management.
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PMID:Daytime sleepiness and myotonic dystrophy. 2343 Jun 86

Neurocysticercosis (NCC) caused by Taenia solium cysts is a frequent but neglected parasitic disease of the central nervous system (CNS) worldwide. The aim of this study was to describe anatomical locations of cysts in the CNS and the corresponding inflammation. A total of 17 naturally infected pigs were used to evaluate the distribution of cysts and, of these, seven were used to evaluate the corresponding inflammation further, through histopathology. Clinical signs in the pigs included dullness, sluggishness, somnolence, apathy and loss of consciousness. Cysts were distributed in all cerebral lobes, i.e. 39.7% in the frontal lobe, 20.3% in the parietal lobe, 20.0% in the occipital lobe and 19.7% in the temporal lobe, and only 0.4% in the cerebellum. No cysts were found in the spinal cord. Cysts were localized as follows: 47.9% in the dorsal subarachnoid, 46.9% in the parenchyma, 4.4% in the subarachnoid base and 0.9% in the ventricles. The results of the histopathology revealed lesions in an early inflammatory stage, i.e. stage I, in all anatomical locations except for two, which showed more of an inflammatory reaction, stage III, in one pig. It was concluded that clinical signs in pigs were neither pathognomonic nor consistent. These signs, therefore, cannot be used as a reliable indicator of porcine NCC. Furthermore, T. solium cysts were found to be in abundance in all cerebral lobes, and only a few were found in the cerebellum. Regarding the inflammatory response, no significant differences were found in the location and total number of cysts. Thus, further studies are needed to explain the determinants of cyst distribution in the CNS and assess in detail clinical signs associated with porcine NCC.
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PMID:Distribution and histopathological changes induced by cysts of Taenia solium in the brain of pigs from Tanzania. 2486 74

Although Parkinson's disease (PD) is diagnosed on the basis of motor symptoms, including slowness of movement, tremor, rigidity and difficulties with balance and walking, now we are aware that non-motor symptoms are highly prevalent, since they can anticipate motor symptoms and can cause severe consequences. Several studies have shown that non-motor symptoms, such as depression, anxiety and apathy, psychosis (e.g., hallucinations, delusions), sleep disturbance, and pain may have a greater adverse impact on quality of life and health economics compared with motor symptoms. Non-motor symptoms can be divided into four domains: neuropsychiatric (e.g., depression, anxiety, apathy, hallucinations, dementia), autonomic (e.g., constipation, orthostatic hypotension, urinary changes, sweating abnormalities), sleep (e.g., insomnia, sleep fragmentation, excessive daytime sleepiness, rapid eye movement, sleep behavioural disorder, restless leg syndrome), and sensory dysfunction (e.g., pain, olfactory dysfunction). This review addresses diagnosis and treatment of these disorders. The causative mechanisms remain complex, since they reflect the widespread brainstem and cortical pathology of PD, with involvement of several neurotransmitters, including dopamine (DA), serotonin, norepinephrine, and acetylcholine. The diagnosis is often challenging, especially for psychiatric disorders, and in particular affective disorders, because somatic features of psychopathology may overlap with the movement disorder itself. Treatments used are limited and psychiatric drugs may not be as effective as in general population. Evidence based medicine is quite poor and it still requires well-designed clinical studies.
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PMID:A clinical overview of non-motor symptoms in Parkinson's Disease. 2487 24

Cognitive alterations accompany or follow motor disorders in subjects with Parkinsonism. The canonical phenotypeof the Parkinson's disease Dementia (PD-D) or Lewy Body Dementia (LBD) includes deficit of attention, executiveand visuospatial functions, and presents often with apathy, hallucinations, delusions, excessive daytime sleepiness,or sleep disorders. However, the clinical expression may overlap with other neurodegenerative diseases associatedwith cognitive disorders. Thus, while clinicians rely on phenomenological patterns to infer the disease causing thecognitive impairment, the inference is weakened by the heterogeneous clinical expression of the disease. In addition,recent post-mortem studies seem to undermine the supposed pathology-phenotype coherence, making it moreand more unreliable the diagnosis based on symptoms. The lack of coherence between phenotype and pathologymay support the speculation about a common mechanism underlying the progression of the disease. While it is verylikely that a distinct, specific causal event determines the disease itself, the progression might well follow commonpatterns. A number of observations suggest that progressive diseases, which cause cognitive impairment, share aprion-like mechanism. A seeding process is supposed to account for the spreading of the lesion.
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PMID:Heterogeneous pathologies associated with dementia in Parkinsonism share a prion-like spreading mechanism. 2487 25

Neurocysticercosis (NCC) caused by Taenia solium cysts is a frequent but neglected parasitic disease of the central nervous system (CNS) worldwide. The aim of this study was to describe anatomical locations of cysts in the CNS and the corresponding inflammation. A total of 17 naturally infected pigs were used to evaluate the distribution of cysts and, of these, seven were used to evaluate the corresponding inflammation further, through histopathology. Clinical signs in the pigs included dullness, sluggishness, somnolence, apathy and loss of consciousness. Cysts were distributed in all cerebral lobes, i.e. 39.7% in the frontal lobe, 20.3% in the parietal lobe, 20.0% in the occipital lobe and 19.7% in the temporal lobe, and only 0.4% in the cerebellum. No cysts were found in the spinal cord. Cysts were localized as follows: 47.9% in the dorsal subarachnoid, 46.9% in the parenchyma, 4.4% in the subarachnoid base and 0.9% in the ventricles. The results of the histopathology revealed lesions in an early inflammatory stage, i.e. stage I, in all anatomical locations except for two, which showed more of an inflammatory reaction, stage III, in one pig. It was concluded that clinical signs in pigs were neither pathognomonic nor consistent. These signs, therefore, cannot be used as a reliable indicator of porcine NCC. Furthermore, T. solium cysts were found to be in abundance in all cerebral lobes, and only a few were found in the cerebellum. Regarding the inflammatory response, no significant differences were found in the location and total number of cysts. Thus, further studies are needed to explain the determinants of cyst distribution in the CNS and assess in detail clinical signs associated with porcine NCC.
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PMID:Distribution and histopathological changes induced by cysts of Taenia solium in the brain of pigs from Tanzania. 2490 52

A 55-year-old woman was admitted with a 3 days history of increasing lethargy with bradyphrenia and apathy. She progressively developed severe somnolence with marked abulia, right hemiparesis, right hemianopsia, and pseudobulbar palsy. Brain magnetic resonance imaging showed the rare image of bilateral acute anterior choroidal artery infarction. Pseudobulbar mutism and in rare cases abulia have been described in acute anterior choroidal artery infarction contralateral to an older lesion in mirror position. Although neurologic deterioration is not infrequent in anterior choroidal artery territory infarcts, the absence of focal neurologic signs on admission is rare and did not raise suspicion of acute stroke.
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PMID:Bilateral anterior choroidal artery infarction presenting with progressive somnolence. 2510 36


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