AGITATION
18 sept. 2019 Causes. - Assessment. - Impact on patient family and MDT Team. - Medical
Understanding agitation
When a person with a mood disorder is agitated friends and family members—or even doctors—can't always tell what underlying condition has caused it. In other
Retrospective Study on Agitation Provoked by Memantine in Dementia
treatment onset; previous episodes of agitation caused by other drugs; type and frequency of comorbidities; distribution of concurrent medications; evidence
Emergence agitation in pediatric anesthesia: current features
purpose of this paper is to discuss the possible causes of postoperative agitation in children providing a foundation for better methods of identifying and
Managing Delirium and Agitation in the Older Emergency
16 juil. 2019 Agitation and delirium are common reasons for older adults to seek care in the emergency department (ED). Providing care for this.
Alzheimers Association
environmental influences and some medications can cause behavioral symptoms or make them worse. These symptoms include: • Sleep disturbances. • Agitation
Changed behaviours and dementia 8 - Agitated behaviours
This help sheet discusses some of the causes of agitated behaviours which can be a very concerning symptom of dementia and suggests ways to prevent and manage
Location of Acute Infarcts and Agitation and Aggression in Stroke
6 oct. 2016 behavior causes damage to individuals or property; atti- ... symptoms15 mixing agitation with anger and hostility
Agitation dans les démences
On doit chercher et traiter les causes réversibles de ces symptômes et décoder le message caché derrière le comportement manifesté. Il faut considérer tout
Guidelines for the management of Behavioural and Psychological
Behavioural and Psychiatric Symptoms of Dementia (BPSD) are a core part of the syndrome of dementia. These include agitation aggression
Acute Agitation - ACEP
ED the cause of agitation is often undifferentiated and can be a consequence of alcohol intoxication drug intoxication psychiatric illness or underlying medical illness Early efforts in the ED should include identifying and treating any reversible causes but in many cases of behavioral disturbance intervention is indicated to reduce the
Agitation and Restlessness: What Causes It? - WebMD
agitation in the medical setting Step 1: Assess situation and cause of agitation • Delirium (make sure underlying medical cause is being addressed) • Intoxication (central nervous system [CNS] stimulant vs depressant) • Primary psychiatric disorder (e g psychosis mania) • Undetermined cause
Managing Delirium and Agitation in the Older Emergency - ACEP
Infections neurologic disorders and metabolic orelectrolyte disorder are 3 of the most common causes ofacute alterations in mental status among older patients 9Adverse medication effects are another common cause Alist of medications that are high risk for causingconfusion altered mental status or delirium is shown in Table 1
Guidelines for the Management of Agitation & Delirium
In addition agitation can be caused by: Pain Urinary retention Anxiety Depression/psychiatric illness Existential distress Drugs in order of use Step 1 Lorazepam or Midazolam Step 2 Benzodiazepine + Levomepromazine Step 3 Midazolam + Levomepromazine + Phenobarbital 6 1 Lorazepam Lorazepam can be given SL PO PR SC IM or IV
Can a medical condition cause agitation?
Agitation is a sense of inner tension and restlessness. When it happens, you may get annoyed easily or feel like you need to move around. It’s a normal emotion. But it’s more likely to show up when you’re under a lot of stress. It can also happen if you use drugs or withdraw from alcohol. But sometimes, a medical condition can cause agitation.
What causes agitation without delirium?
Both have a number of possible underlying causes and these overlap. Agitation without delirium can occur as a result of anxiety or psychological/spiritual distress and commonly due to unrelieved constipation or urinary retention. This policy advocates a ‘THINK DELIRIUM’and STEPWISE approach.
Is agitation the same as aggression?
You may act angry or violent at the same time. But agitation isn’t the same as aggression. It’s also different than akathisia. That’s a movement disorder often caused by antipsychotic medication. It’s normal to get worried if you or a loved one is agitated a lot. But your doctor can help you find and treat the cause.
Can hypothyroidism cause agitation?
Treatment for your hypothyroidism should ease your agitation. Your doctor will give you medicine to bring your hormone levels back to normal. Hormone changes before your period can make you feel tense. But you may get really overwhelmed and agitated if you have premenstrual dysphoric disorder (PMDD).
Retrospective Study on Agitation Provoked by
Memantine in Dementia
Fulvio Da Re, M.D., Francesco Rucci, M.D., Valeria Isella, M.D., Ph.D.The authors retrospectively reviewed the clinical records of 196 patients with dementia treated with memantine for at least 6
months. Eleven (5.6%) developed treatment-induced agitation. At chi-square analysis, they were significantly more likely to
have a history of similar side effects from other medications acting on the central nervous system in comparison with the
group without agitation, suggesting neurochemical susceptibility. A trend toward a significantly greater prevalence was also
present for ischemic cardiopathy and neuroimaging evidence of chronic small vessel disease. Ischemic brain and heart
disease might contribute through anatomical and functional alterations within the glutamatergic system.
J Neuropsychiatry Clin Neurosci 2015; 27:e10-e13; doi: 10.1176/appi.neuropsych.13100226TheN-methyl-D-aspartic acid (NMDA) receptor antagonist
memantine (Ebixa; Lundbeck Canada, Montreal, Canada) has aggressiveness in Alzheimer'sdisease(AD), 1-3 hypothetically via correction of glutamate transmission and reduction of tangle formation in the frontal and cingulate cortices. 4,5 Con- versely, memantine has been shown to cause agitation and other psychotic manifestations. A total of 11 cases of AD,6,7Lewy body disease,
8-10 and Parkinson's disease 11 have been reported who developed agitation, hallucinations, delusions, and intense dreaming after a few doses and recovered at drug withdrawal. This apparently paradoxical effect of memantine has a neurochemical plausibility. The NMDA hypofunction within the limbic system is deemed to underlie psychotic disorders,5 other glutamate receptor antagonists such as amantadine and phencyclidine. In the present study, we retrospectively reviewed the clin- ical records of a large sample of patients with dementia treated with memantine, with the aim to measure the prevalence of treatment-emergent agitation in naturalistic conditions and identify possible clinical correlates of this puzzling effect of the drug.PATIENTS AND METHODS
Participants were enrolled from the memory clinic of S. Gerardo Hospital, Monza, Italy. They were consecutive pa- tients started on memantinebetween January 2008 and December 2010 and followed up for at least 6 months since dementia according to DSM IV criteria.12 The study hadthe relevant institutional ethical approval and complied with the Declaration of Helsinki. dailydoseof 20mgwasusuallyachieved byupwardtitration of 5 mg/week over a period of 3 weeks. Agitation, restlessness, irritability, and aggressiveness re- portedby patients orinformantswere all recordedas agitation; co-occurrence of confusion, hallucinations, and delusions was also taken into account. The symptoms were deemed to be drug related when they developed de novo or worsened if already present at study entry, in temporal relationship with treatment start or increase, and resolved after dose reduction or withdrawal. The following characteristics of patients with (A+) and without (A2) memantine-related agitation were compared using two-tailed Student's t or chi-square tests: percentage of AD and non-AD diagnoses; Mini Mental State Examination (MMSE) score; presence of neuropsychiatric disturbances at treatment onset; previous episodes of agitation caused by of concurrent medications; evidence of chronic small vessel disease at the visual rating of brain CT or MRI scans by the neuroradiologist. The level of significance was set at p,0.05, and Bonferroni correction for multiple comparisons was ap-Release Version 18.0.0 (SPSS, Chicago, IL).
RESULTS
A total of 209 cases meeting inclusion criteria were identi- fied, but 13 had to be excluded due to inadequate data. Of the196 cases included in thefinal sample, 11 (5.6%) showede10neuro.psychiatryonline.org J Neuropsychiatry Clin Neurosci 27:1, Winter 2015
ARTICLES
memantine-related agitation, and their demographic and clinical features are shown in Table 1. The remaining 185 patients were 70 men (38%) and 115 score of 16.965.0 and had the following diagnoses, based on current criteria 13-18 : AD (n=113, 61%), vascular or mixed de- mentia (n=21, 11%), Lewy body dementia (n=16, 9%), fronto- temporal dementia (n=13, 7%),corticobasal degeneration (n=8, 4%), nonotherwise specified dementia (n=8, 4%), and posterior cortical atrophy (n=6, 3%). Within this A2group,148 patients (80%) showed mild (n=71, 38%) or moderate to
severe (n=77, 42%) behavioral disturbances at the time they were started on memantine. After 2.161.1 years of treatment on average, an improvement of agitation was reported by the clinician, based on informants'reports, for 28 cases (19%). A brief description of the adverse events with memantine is reported in Table 1. Infive of 11 (45.5%) patients, agitation developed de novo, whereas in the other six patients, it was preexisting and worsened after drug introduction. In four cases (36.4%), it was associated with confusion, and in one patient (9.1%), it was associated with de novo visual hallu- cinations. The adverse effects became evident after thefirst doses in seven cases (63.6%) and when the daily dose was increased to 10 mg or above in the other four patients. Mem- antine was reduced to 10 mg/day in two cases (18.2%) and was withdrawn in all the others, with a complete remission of the adverse effects within a few days. No A+ patient completedmorethan 2 weeks at 20 mg. In case 7, the drug was tentativelyreintroduced 18 months later, with a slower increase to 20
mg, but again had to be discontinued due to agitation and confusion. Within the study follow-up period (2.261.0 years on aver- age), a total of 22 adverse effects tentatively attributed to memantinewerealsoobservedintheA2group, the most frequent (3.6%) being a vague feeling of"being unwell"TABLE 1. Characteristics of Patients Who Developed Agitation as an Adverse Event of Treatment With Memantine
a Patient N Sex/Age-Diagnosis MMSE Score Description of Event1 F/83-AD 9 Preexisting agitation worsens soon after thefirst 5-mg doses. The treatment is
withdrawn after 1 week at 10 mg.2 F/83-AD 10 The patient shows progressive exacerbation of agitation during memantine
titration. The treatment is discontinued after a few days at 20 mg.3 F/77-AD 14 Due to an error in following the prescription, the dose of memantine is
maintained at 10 mg for 6 months. The increase to 20 mg causes agitation and confusion within a couple of days, and the dose is brought back to 10 mg.4 M/66-AD NA The patient is agitated and aggressive at treatment start, and gradually worsens
during memantine increase up to 20 mg. The drug is discontinued approximately after 5 weeks since its introduction.5 M/81-AD 19 De novo agitation develops immediately after thefirst 5-mg doses. The drug is
withdrawn after 1 week at 10 mg.6 M/81-AD 21 The patient is mildly agitated at treatment start and remains stable up to 10 mg
of memantine. A few days at 20 mg cause severe agitation and the dose is reduced. Preexisting hallucinations and delusions remain unchanged.7 M/85-AD 21 The patient becomes increasingly agitated and confused during the titration to
20 mg, and the treatment is discontinued within a few weeks.
8 F/96-AD 13 Progressive confusion and exacerbation of agitation occur since treatment start.
The drug is withdrawn after 1 week at 15 mg. Preexisting hallucinations and delusions are apparently unchanged.9 M/77-AD 9 Agitation and confusion develop within thefirst days at 5 mg, and treatment is
discontinued 10 days later.10 M/63-PCA 9 Preexisting agitation worsens after less than 1 week at 20 mg, and memantine is
discontinued 20 days later.11 M/74-LBD 20 Agitation and de novo visual hallucinations develop soon after the increase to
10 mg. The treatment is discontinued 10 days after its introduction.
aIn all cases, memantine discontinuation or reduction was followed by complete remission of symptoms. AD: Alzheimer's disease; F: female; LBD: Lewy body
disease; NA: not administered (due to agitation); M: male; MMSE: Mini Mental State Examination; PCA: posterior cortical atrophy.
TABLE 2. Adverse Events of Memantine and Causes of Discontinuation Other Than Treatment Side Effects in the Group of 185 Patients Who Did Not Develop AgitationVariable N Percentage
Adverse events
Aspecific malaise 7 3.6
Dizziness 4 2.0
Sedation 4 2.0
Asthenia 2 1.0
Hypertension 2 1.0
Constipation 2 1.0
Chronic cough 1 0.5
Total 22 11.2
Causes of discontinuation
Disease progression 17 8.7
Institutionalization 12 6.1
Medical or surgical conditions
(unrelated to memantine)7 3.6Unknown 4 2.0
Total 45 23.0
Absolute number and percentage of events are calculated in the whole study population (11 patients with agitation + 185 patients without agitation). J Neuropsychiatry Clin Neurosci 27:1, Winter 2015 neuro.psychiatryonline.orge11DA RE ET AL.
(Table 2). Because of these side effects, treatment was withdrawn or reduced in 20 (10.2%) cases. Discontinuation also occurred in 45 (23%) other A2patients for reasons other than adverse events, e.g., disease progression (Table 3). The mean duration of treatment was 2.061.2 years for theA2group (range: 1 month to 5.3 years).
Results of comparison analysis for demographic and clin- ical features of A+ and A2patientsareshowninTable3. After Bonferroni correction, a statistically significant dif- ference (p=0.001) was found fora greater frequency, in the A+ group, of past episodes of agitation in response to other drugs (rivastigmine in one patient, donepezil in another case,donepezil and citicoline in a third patient, and piracetam inone last case). A strong trend toward signifi-
cance was present for a higher prevalence of brain small vessel disease and ischemic cardi- opathy (36.4% versus 6.5%, p=0.007, for both), whereas no difference emerged in the distri- bution of related medications. There was no case of overlap of the three more significant variables in the A+ group; only one of four patients with cerebrovascular disease also showed ischemic cardiopathy, and only twoof four patients taking anticholinesterase inhibitors also showed one of the two disorders. This suggests an independent contribution for the three features.The 28 cases who showed improvement in
behavioral disturbances after starting memantine did not differ from the A+ group for the fol- lowing features: age, gender, education, distri- bution of diagnoses, disease duration, MMSE score, percentage of patients treated with an- ticholinesterase inhibitors or other neuropsychi- atric drugs, and prevalence of non-neurological trend toward significance was only present for a higher proportion of A+ cases showing brain small vessel disease at neuroimaging (36.4% versus 7.1%, p=0.042).DISCUSSION
The retrospective nature of our studyand the
lack of structured measures of safety (e.g., a neuropsychiatric scale) did not allow a sys- tematic,fine-grained, and standardized col- lection of data. Moreover, being unblinded to treatment, we may have been biased in estab- lishing a causal relationship between meman- tine and agitation. Also, the absolute number of cases showing the adverse effects was small and allowed only an exploratory analysis of features comparisons. Finally, errors in the presumed clinical diagnoses cannot be ruled out, and might have affected our results be- cause the underlying pathological diagnosis may be a risk factor for the development of memantine- induced agitation. On the other hand, the entire study population was rel- atively large and was studied in a naturalistic setting, which guarantees a realistic and clinically relevant depiction of the event under investigation. Therefore, we believe that useful indications for future studies may come from our results, along with some hint for clinical practice. In particular, we highlighted some feature that may help dementia specialists to identify patients at risk of developing neuropsychiatric side effects of memantine. A redflag seems to be a history of agitation in reaction to brain enhancers. Informants should be specifically inquired about that before TABLE 3. Demographic and Clinical Features of the 11 Patients Who Developed Agitation as an Adverse Effect of Memantine Compared With the Rest of theStudy Population
aPatients With
Agitation
(N=11)Patients WithoutAgitation
(N=185) t test/x 2 pAge (mean6SD) 79.168.6 77.368.0-0.680 0.511
Sex (men) 63.6% 37.8% 2.897 0.085
MMSE (mean6SD) 14.565.3 16.965.0-1.395 0.193
Dementia of the
Alzheimer type
b91.0% 68.1% 2.541 0.098
Preexisting BPSD 63.6% 81.6% 2.149 0.142
Cerebral chronic small
vessel disease36.4% 6.5% 12.363 0.007Ischemic cardiopathy 37.6% 6.5% 12.363 0.007
Agitation with past
medications36.4% 2.8% 26.205 0.001Concomitant AChE
inhibitors36.4% 37.3% 0.004 0.610Drugs active on the CNS
cAntidepressants 92.9% 79.9% 1.607 0.182
Antipsychotics 43.9% 40.0% 0.897 0.684
Others 23.0% 33.0% 2.001 0.132
Other medications
Antihypertensives 65.5% 53.2% 2.648 0.165
Cardiological drugs 54.6% 36.2% 1.980 0.155
Cholesterol lowering
drugs45.5% 24.6% 3.238 0.100Antidiabetics 18.2% 9.7% 0.809 0.311
Others 35.7% 36.7% 0.041 0.599
Treatment with more than
one drug90.9% 87.0% 0.141 0.578History of stroke/TIA 9.1% 5.9% 0.179 0.510
Non vascular neurological
disorders9.1% 10.3% 0.016 0.689Vascular risk factors
d90.9% 58.4% 4.586 0.028
Cancer 9.1% 10.3% 0.016 0.689
Atrialfibrillation 54.5% 16.2% 10.173 0.006
Other heart-diseases
e0.0% 3.2% 0.368 0.704
Lung diseases 9.1% 6.5% 0.114 0.540
Digestive system diseases 45.5% 14.6% 7.238 0.019
Other comorbidities 36.4% 23.2% 0.980 0.255
a All values are percentage of cases, unless otherwise stated. AChE: anticholinesterase; BPSD: Behavioral and Psychological Symptoms of Dementia; CNS: central nervous system; MMSE: Mini Mental State Examination; TIA: transient ischemic attack. b Including patients with posterior cortical atrophy. cExcluding anticholinesterase inhibitors.
d Carotid stenosis, hypertension, diabetes, hypercholesterolemia. eExcluding ischemic cardiopathy.
e12neuro.psychiatryonline.org J Neuropsychiatry Clin Neurosci 27:1, Winter 2015AGITATION CAUSED BY MEMANTINE
treatment start. Evidence of chronic microvascular changes at neuroimaging and presence of coronary heart disease (more precisely, a history and/or electrocardiographic or echocardiographic evidenceofmiocardialinfarction)should concomitant medications do not necessarily entail a more careful monitoring of the patient once he/she is started on memantine. The fact that A+ patients showed the same side effects in response to other medications acting on the central nervous system suggests that some subject might have a neurochem- ical predisposition to develop the adverse event. Following the glutamate model of psychosis, 5 it could be hypothesized that a low baseline glutamatergic tone might make them more vulnerable to the psychosis-inducing effect of the NMDA antagonist. Cerebrovascular damage and ischemic cardiopathy are known to causeanatomical and functional changes in the brain.quotesdbs_dbs35.pdfusesText_40[PDF] fiche les solides gs
[PDF] solides maternelle
[PDF] figure geometrique liste
[PDF] les différentes écritures dun nombre ce1
[PDF] schéma fécondation humaine
[PDF] schéma fécondation nidation
[PDF] expression francaise a mimer
[PDF] expressions françaises drôles
[PDF] les gestes de salutation dans le monde
[PDF] physiopathologie de lépilepsie
[PDF] cours epilepsie ppt
[PDF] epilepsie cours
[PDF] epilepsie signes cliniques
[PDF] nom des excipients ? l'origine d'effets secondaires
