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Agitation

MedGen UID:
88447
Concept ID:
C0085631
Sign or Symptom
Synonyms: Agitated; Agitated behavior; Feeling agitated; Psychomotor agitation; Unable to keep still
SNOMED CT: Agitation (24199005); Agitated behavior (24199005); Feeling agitated (24199005); Agitated (24199005); Unable to keep still (24199005)
 
HPO: HP:0000713

Definition

A state of extreme restlessness and excessive motor activity is associated with mental distress or a feeling of inner tension. [from HPO]

Conditions with this feature

Mucopolysaccharidosis, MPS-III-D
MedGen UID:
88602
Concept ID:
C0086650
Disease or Syndrome
Mucopolysaccharidosis type III (MPS III) is a multisystem lysosomal storage disease characterized by progressive central nervous system degeneration manifest as severe intellectual disability (ID), developmental regression, and other neurologic manifestations including autism spectrum disorder (ASD), behavioral problems, and sleep disturbances. Disease onset is typically before age ten years. Disease course may be rapidly or slowly progressive; some individuals with an extremely attenuated disease course present in mid-to-late adulthood with early-onset dementia with or without a history of ID. Systemic manifestations can include musculoskeletal problems (joint stiffness, contractures, scoliosis, and hip dysplasia), hearing loss, respiratory tract and sinopulmonary infections, and cardiac disease (valvular thickening, defects in the cardiac conduction system). Neurologic decline is seen in all affected individuals; however, clinical severity varies within and among the four MPS III subtypes (defined by the enzyme involved) and even among members of the same family. Death usually occurs in the second or third decade of life secondary to neurologic regression or respiratory tract infections.
Sulfite oxidase deficiency
MedGen UID:
78695
Concept ID:
C0268624
Disease or Syndrome
The spectrum of isolated sulfite oxidase deficiency ranges from classic early-onset (severe) disease to late-onset (mild) disease. Classic ISOD is characterized in the first few hours to days of life by intractable seizures, feeding difficulties, and rapidly progressive encephalopathy manifest as abnormal tone (especially opisthotonus, spastic quadriplegia, and pyramidal signs) followed by progressive microcephaly and profound intellectual disability. Lens subluxation or dislocation, another characteristic finding, may be evident after the newborn period. Children usually die during the first few months of life. Late-onset ISOD manifests between ages six and 18 months and is characterized by ectopia lentis (variably present), developmental delay/regression, movement disorder characterized by dystonia and choreoathetosis, ataxia, and (rarely) acute hemiplegia as a result of metabolic stroke. The clinical course may be progressive or episodic. In the episodic form encephalopathy, dystonia, choreoathetosis, and/or ataxia are intermittent.
FRAXE
MedGen UID:
155512
Concept ID:
C0751157
Disease or Syndrome
Intellectual developmental disorder-109 (MRX109) is characterized by mildly to moderately impaired intellectual development associated with learning difficulties, communication deficits, attention problems, hyperactivity, and autistic behavior (summary by Bensaid et al., 2009). The disorder, which is associated with a fragile site on chromosome Xq28 (FRAXE), can be caused either by silencing of the FMR2 gene as a consequence of a CCG expansion located upstream of this gene or by deletion within the gene (Stettner et al., 2011).
Intellectual disability, X-linked 30
MedGen UID:
163235
Concept ID:
C0796237
Disease or Syndrome
Any non-syndromic X-linked intellectual disability in which the cause of the disease is a mutation in the PAK3 gene.
Migraine, familial hemiplegic, 1
MedGen UID:
331388
Concept ID:
C1832884
Disease or Syndrome
Familial hemiplegic migraine (FHM) falls within the category of migraine with aura. In migraine with aura (including FHM) the neurologic symptoms of aura are unequivocally localizable to the cerebral cortex or brain stem and include visual disturbance (most common), sensory loss (e.g., numbness or paresthesias of the face or an extremity), and dysphasia (difficulty with speech). FHM must include motor involvement, such as hemiparesis (weakness of an extremity). Hemiparesis occurs with at least one other symptom during FHM aura. Neurologic deficits with FHM attacks can be prolonged for hours to days and may outlast the associated migrainous headache. FHM is often earlier in onset than typical migraine, frequently beginning in the first or second decade; the frequency of attacks tends to decrease with age. Approximately 40%-50% of families with CACNA1A-FHM have cerebellar signs ranging from nystagmus to progressive, usually late-onset mild ataxia.
Microcephaly with or without chorioretinopathy, lymphedema, or intellectual disability
MedGen UID:
320559
Concept ID:
C1835265
Disease or Syndrome
Microcephaly with or without chorioretinopathy, lymphedema, or impaired intellectual development (MCLMR) is an autosomal dominant disorder that involves an overlapping but variable spectrum of central nervous system and ocular developmental anomalies. Microcephaly ranges from mild to severe and is often associated with mild to moderate developmental delay and a characteristic facial phenotype with upslanting palpebral fissures, broad nose with rounded tip, long philtrum with thin upper lip, prominent chin, and prominent ears. Chorioretinopathy is the most common eye abnormality, but retinal folds, microphthalmia, and myopic and hypermetropic astigmatism have also been reported, and some individuals have no overt ocular phenotype. Congenital lymphedema, when present, is typically confined to the dorsa of the feet, and lymphoscintigraphy reveals the absence of radioactive isotope uptake from the webspaces between the toes (summary by Ostergaard et al., 2012). Robitaille et al. (2014) found that MCLMR includes a broader spectrum of ocular disease, including retinal detachment with avascularity of the peripheral retina, and noted phenotypic overlap with familial exudative vitreoretinopathy (FEVR; see EVR1, 133780). Birtel et al. (2017) observed intrafamilial and intraindividual variability in retinal phenotype, and noted that syndromic manifestations in some patients are too subtle to be detected during a routine ophthalmologic evaluation. Variable expressivity and reduced penetrance have also been observed in some families (Jones et al., 2014; Li et al., 2016). Autosomal recessive forms of microcephaly with chorioretinopathy have been reported (see 251270). See also Mirhosseini-Holmes-Walton syndrome (autosomal recessive microcephaly with pigmentary retinopathy and impaired intellectual development; 268050), which has been mapped to chromosome 8q21.3-q22.1.
GRN-related frontotemporal lobar degeneration with Tdp43 inclusions
MedGen UID:
375285
Concept ID:
C1843792
Disease or Syndrome
The spectrum of GRN frontotemporal dementia (GRN-FTD) includes the behavioral variant (bvFTD), primary progressive aphasia (PPA; further subcategorized as progressive nonfluent aphasia [PNFA] and semantic dementia [SD]), and movement disorders with extrapyramidal features such as parkinsonism and corticobasal syndrome (CBS). A broad range of clinical features both within and between families is observed. The age of onset ranges from 35 to 87 years. Behavioral disturbances are the most common early feature, followed by progressive aphasia. Impairment in executive function manifests as loss of judgment and insight. In early stages, PPA often manifests as deficits in naming, word finding, or word comprehension. In late stages, affected individuals often become mute and lose their ability to communicate. Early findings of parkinsonism include rigidity, bradykinesia or akinesia (slowing or absence of movements), limb dystonia, apraxia (loss of ability to carry out learned purposeful movements), and disequilibrium. Late motor findings may include myoclonus, dysarthria, and dysphagia. Most affected individuals eventually lose the ability to walk. Disease duration is three to 12 years.
Growth delay due to insulin-like growth factor I resistance
MedGen UID:
338622
Concept ID:
C1849157
Disease or Syndrome
Patients with mutations in the receptor for insulin-like growth factor I show intrauterine growth retardation and postnatal growth failure, resulting in short stature and microcephaly. Other features may include delayed bone age, developmental delay, and dysmorphic features.
ACTH-independent macronodular adrenal hyperplasia 1
MedGen UID:
347456
Concept ID:
C1857451
Disease or Syndrome
ACTH-independent macronodular adrenal hyperplasia (AIMAH) is an endogenous form of adrenal Cushing syndrome characterized by multiple bilateral adrenocortical nodules that cause a striking enlargement of the adrenal glands. Although some familial cases have been reported, the vast majority of AIMAH cases are sporadic. Patients typically present in the fifth or sixth decade of life, approximately 10 years later than most patients with other causes of Cushing syndrome (Swain et al., 1998; Christopoulos et al., 2005). Approximately 10 to 15% of adrenal Cushing syndrome is due to primary bilateral ACTH-independent adrenocortical pathology. The 2 main subtypes are AIMAH and primary pigmented nodular adrenocortical disease (PPNAD; see 610489), which is often a component of the Carney complex (160980) and associated with mutations in the PRKAR1A gene (188830). AIMAH is rare, representing less than 1% of endogenous causes of Cushing syndrome (Swain et al., 1998; Christopoulos et al., 2005). See also ACTH-independent Cushing syndrome (615830) due to somatic mutation in the PRKACA gene (601639). Cushing 'disease' (219090) is an ACTH-dependent disorder caused in most cases by pituitary adenomas that secrete excessive ACTH. Genetic Heterogeneity of ACTH-Independent Macronodular Adrenal Hyperplasia AIMAH2 (615954) is caused by germline mutation on 1 allele of the ARMC5 gene (615549) coupled with a somatic mutation in the other allele.
Cluster headache, familial
MedGen UID:
350040
Concept ID:
C1861513
Disease or Syndrome
The Headache Classification Committee of the International Headache Society (1988) listed the following criteria for cluster headache (CH): at least 5 attacks of severe unilateral orbital, supraorbital, and/or temporal pain, lasting 15 to 180 minutes, associated with at least 1 of 8 local autonomic signs, and occurring once every other day to 8 per day. Approximately 85% of CH patients have the episodic subtype, in which the headaches occur in cluster periods lasting from 7 days to 1 year and separated by attack-free intervals of 1 month or more. The remainder of patients have the chronic subtype, in which attacks recur for greater than 1 year without remission or with remissions lasting less than 1 month (Lipton et al., 2004).
Pigmented nodular adrenocortical disease, primary, 1
MedGen UID:
400627
Concept ID:
C1864846
Disease or Syndrome
Primary pigmented nodular adrenocortical disease (PPNAD) is a form of ACTH-independent adrenal hyperplasia resulting in Cushing syndrome. It is usually seen as a manifestation of the Carney complex (CNC1; 160980), a multiple neoplasia syndrome. However, PPNAD can also occur in isolation (Groussin et al., 2002). Genetic Heterogeneity of Primary Pigmented Nodular Adrenocortical Disease See also PPNAD2 (610475), caused by mutation in the PDE11A gene (604961) on chromosome 2q31; PPNAD3 (614190), caused by mutation in the PDE8B gene (603390) on chromosome 5q13; and PPNAD4 (615830), caused by a duplication on chromosome 19p13 that includes the PRKACA gene (601639).
Pigmented nodular adrenocortical disease, primary, 2
MedGen UID:
355843
Concept ID:
C1864851
Disease or Syndrome
Any primary pigmented nodular adrenocortical disease in which the cause of the disease is a mutation in the PDE11A gene.
Hereditary spastic paraplegia 4
MedGen UID:
401097
Concept ID:
C1866855
Disease or Syndrome
Spastic paraplegia 4 (SPG4; also known as SPAST-HSP) is characterized by insidiously progressive bilateral lower-limb gait spasticity. More than 50% of affected individuals have some weakness in the legs and impaired vibration sense at the ankles. Sphincter disturbances are very common. Onset is insidious, mostly in young adulthood, although symptoms may start as early as age one year and as late as age 76 years. Intrafamilial variation is considerable.
Wilms tumor, aniridia, genitourinary anomalies, intellectual disability, and obesity syndrome
MedGen UID:
382718
Concept ID:
C2675904
Disease or Syndrome
For a detailed discussion of the WAGR syndrome, see 194072. In a subgroup of individuals with the WAGR syndrome, obesity develops. The phenotype in this subset is associated with haploinsufficiency for the BDNF gene.
Hirschsprung disease, cardiac defects, and autonomic dysfunction
MedGen UID:
462587
Concept ID:
C3151237
Disease or Syndrome
HSD10 mitochondrial disease
MedGen UID:
781653
Concept ID:
C3266731
Disease or Syndrome
HSD10 mitochondrial disease (HSD10MD) most commonly presents as an X-linked neurodegenerative disorder with highly variable severity and age at onset ranging from the neonatal period to early childhood. The features are usually multisystemic, consistent with mitochondrial dysfunction. Some affected males have a severe infantile form associated with cardiomyopathy that may result in death in early childhood, whereas other rare patients may have juvenile onset or even atypical presentations with normal neurologic development. More severely affected males show developmental regression in infancy or early childhood, often associated with early-onset intractable seizures, progressive choreoathetosis and spastic tetraplegia, optic atrophy or retinal degeneration resulting in visual loss, and mental retardation. Heterozygous females may show non-progressive developmental delay and intellectual disability, but may also be clinically normal. Although the diagnosis can be aided by the observation of increased urinary levels of metabolites of isoleucine breakdown (2-methyl-3 hydroxybutyrate and tiglylglycine), there is not a correlation between these laboratory features and the phenotype. In addition, patients do not develop severe metabolic crises in the neonatal period as observed in other organic acidurias, but may show persistent lactic acidosis, most likely reflecting mitochondrial dysfunction (summary by Rauschenberger et al., 2010; Zschocke, 2012). In a review of this disorder, Zschocke (2012) noted that although it was originally thought to be an inborn error of branched-chain fatty acid and isoleucine metabolism resulting from decreased HSD17B10 dehydrogenase activity (HSD17B10 'deficiency'), subsequent studies have shown that the HSD17B10 gene product has additional functions and also acts as a component of the mitochondrial RNase P holoenzyme, which is involved in mitochondrial tRNA processing and maturation and ultimately mitochondrial protein synthesis. The multisystemic features of HSD10MD most likely result from the adverse effect of HSD17B10 mutations on mitochondrial function, rather than from the effects on the dehydrogenase activity (see PATHOGENESIS).
Vasculitis due to ADA2 deficiency
MedGen UID:
854497
Concept ID:
C3887654
Disease or Syndrome
Adenosine deaminase 2 deficiency (DADA2) is a complex systemic autoinflammatory disorder in which vasculopathy/vasculitis, dysregulated immune function, and/or hematologic abnormalities may predominate. Inflammatory features include intermittent fevers, rash (often livedo racemosa/reticularis), and musculoskeletal involvement (myalgia/arthralgia, arthritis, myositis). Vasculitis, which usually begins before age ten years, may manifest as early-onset ischemic (lacunar) and/or hemorrhagic strokes, or as cutaneous or systemic polyarteritis nodosa. Hypertension and hepatosplenomegaly are often found. More severe involvement may lead to progressive central neurologic deficits (dysarthria, ataxia, cranial nerve palsies, cognitive impairment) or to ischemic injury to the kidney, intestine, and/or digits. Dysregulation of immune function can lead to immunodeficiency or autoimmunity of varying severity; lymphadenopathy may be present and some affected individuals have had lymphoproliferative disease. Hematologic disorders may begin early in life or in late adulthood, and can include lymphopenia, neutropenia, pure red cell aplasia, thrombocytopenia, or pancytopenia. Of note, both interfamilial and intrafamilial phenotypic variability (e.g., in age of onset, frequency and severity of manifestations) can be observed; also, individuals with biallelic ADA2 pathogenic variants may remain asymptomatic until adulthood or may never develop clinical manifestations of DADA2.
Intellectual disability, autosomal recessive 46
MedGen UID:
863720
Concept ID:
C4015283
Mental or Behavioral Dysfunction
Any autosomal recessive non-syndromic intellectual disability in which the cause of the disease is a mutation in the NDST1 gene.
Intellectual disability-epilepsy-extrapyramidal syndrome
MedGen UID:
934650
Concept ID:
C4310683
Disease or Syndrome
Neurodevelopmental disorder with hypotonia and impaired expressive language and with or without seizures (NEDHELS) is an autosomal recessive disorder characterized by hypotonia, poor feeding, and global developmental delay apparent from infancy. Most patients have poor overall growth, poor eye contact, sleep disturbances, and severely impaired expressive language. Affected individuals also tend to have behavioral problems, microcephaly, and variable dysmorphic features; many develop seizures. Brain imaging may show enlarged ventricles, thin corpus callosum and brainstem, and white matter abnormalities. The phenotype is variable (summary by Nabais Sa et al., 2019).
Developmental and epileptic encephalopathy, 47
MedGen UID:
934652
Concept ID:
C4310685
Disease or Syndrome
Developmental and epileptic encephalopathy-47 (DEE47) is a neurologic disorder characterized by onset of intractable seizures in the first days or weeks of life. EEG shows background slowing and multifocal epileptic spikes, and may show hypsarrhythmia. Most patients have developmental regression after seizure onset and show persistent intellectual disability and neurologic impairment, although the severity is variable. Treatment with phenytoin, a voltage-gated sodium channel blocker, may be beneficial (summary by Guella et al., 2016). For a general phenotypic description and a discussion of genetic heterogeneity of DEE, see 308350.
Lopes-Maciel-Rodan syndrome
MedGen UID:
1379711
Concept ID:
C4479491
Disease or Syndrome
Neurodevelopmental disorder with poor language and loss of hand skills
MedGen UID:
1637031
Concept ID:
C4693546
Disease or Syndrome
NDPLHS is an autosomal dominant disorder characterized by developmental stagnation or regression apparent in the first years of life and manifest as loss of purposeful hand movements, loss of language, and intellectual disability. Additional features may include stereotypic movements, dystonia, gait abnormalities, sleep disturbances, and small hands and feet. The phenotype is reminiscent of Rett syndrome (RTT; 312750) (summary by Yoo et al., 2017).
Neurodevelopmental disorder with cerebellar atrophy and with or without seizures
MedGen UID:
1648373
Concept ID:
C4748032
Disease or Syndrome
Neurodevelopmental disorder with cerebellar atrophy and with or without seizures (NEDCAS) is an autosomal recessive disorder characterized by intellectual disability associated with ataxia (summary by Engel et al., 2023).
Infantile cataract, skin abnormalities, glutamate excess, and impaired intellectual development
MedGen UID:
1673640
Concept ID:
C5193037
Disease or Syndrome
Aside from the clinical features of infantile cataract, skin abnormalities, and impaired intellectual development, CASGID is characterized by strikingly high intracerebral and urinary glutamate excess with almost undetectable glutamine. A gain-of-function mutation in the GLS gene was found (see MOLECULAR GENETICS) (Rumping et al., 2019). GLS loss of function is implicated in developmental and epileptic encephalopathy-71 (DEE71; 618328) and a syndrome of global developmental delay and progressive ataxia (GDPAG; 618412).
Alopecia-intellectual disability syndrome 4
MedGen UID:
1713432
Concept ID:
C5394241
Disease or Syndrome
Alopecia-intellectual disability syndrome-4 (APMR4) is characterized by alopecia universalis, scaly skin, and psychomotor retardation of varying degrees (Besnard et al., 2019). For a discussion of genetic heterogeneity of alopecia-intellectual disability syndrome, see APMR1 (203650).
Mitochondrial complex 4 deficiency, nuclear type 3
MedGen UID:
1764816
Concept ID:
C5436682
Disease or Syndrome
Mitochondrial complex IV deficiency nuclear type 3 (MC4DN3) is an autosomal recessive multisystem metabolic disorder with a highly variable phenotype. Some patients present with encephalomyopathic features in early infancy, whereas others may present later in infancy or the first years of life after normal early development. Affected individuals show hypotonia, failure to thrive, and developmental delay or regression with poor eye contact and loss of motor skills with ataxia. Additional features observed in some patients include proximal renal tubulopathy, macrocytic anemia, sensorineural hearing loss, nystagmus, and hypertrophic cardiomyopathy, consistent with systemic involvement. Brain imaging in most patients shows lesions consistent with Leigh syndrome (see 256000). Laboratory studies show increased serum lactate and decreased levels and activity of mitochondrial respiratory complex IV. Most patients die in infancy (summary by Valnot et al., 2000 and Antonicka et al., 2003). For a discussion of genetic heterogeneity of mitochondrial complex IV (cytochrome c oxidase) deficiency, see 220110.
Kohlschutter-Tonz syndrome-like
MedGen UID:
1781649
Concept ID:
C5543202
Disease or Syndrome
Den Hoed-de Boer-Voisin syndrome (DHDBV) is characterized by global developmental delay with moderately to severely impaired intellectual development, poor or absent speech, and delayed motor skills. Although the severity of the disorder varies, many patients are nonverbal and have hypotonia with inability to sit or walk. Early-onset epilepsy is common and may be refractory to treatment, leading to epileptic encephalopathy and further interruption of developmental progress. Most patients have feeding difficulties with poor overall growth and dysmorphic facial features, as well as significant dental anomalies resembling amelogenesis imperfecta. The phenotype is reminiscent of Kohlschutter-Tonz syndrome (KTZS; 226750). More variable features of DHDBV include visual defects, behavioral abnormalities, and nonspecific involvement of other organ systems (summary by den Hoed et al., 2021).
Developmental delay, impaired speech, and behavioral abnormalities
MedGen UID:
1794167
Concept ID:
C5561957
Disease or Syndrome
Developmental delay, impaired speech, and behavioral abnormalities (DDISBA) is characterized by global developmental delay apparent from early childhood. Intellectual disability can range from mild to severe. Additional variable features may include dysmorphic facial features, seizures, hypotonia, motor abnormalities such as Tourette syndrome or dystonia, and hearing loss (summary by Cousin et al., 2021).
Neurodevelopmental disorder with hyperkinetic movements and dyskinesia
MedGen UID:
1794248
Concept ID:
C5562038
Disease or Syndrome
Neurodevelopmental disorder with hyperkinetic movements and dyskinesia (NEDHYD) is an autosomal recessive complex neurologic disorder characterized by severe global developmental delay with axial hypotonia, impaired intellectual development, poor overall growth, and abnormal involuntary hyperkinetic movements, including dystonia, myoclonus, spasticity, and orofacial dyskinesia. It is the most severe manifestation of ADCY5-related dyskinetic disorders (summary by Okamoto et al., 2021 and Kaiyrzhanov et al., 2021).
DeSanto-Shinawi syndrome due to WAC point mutation
MedGen UID:
1841517
Concept ID:
C5681129
Disease or Syndrome
WAC-related intellectual disability (ID) is typically characterized by variable degrees of developmental delay and/or intellectual disability. Behavioral abnormalities including anxiety, attention-deficit/hyperactivity disorder, and/or autism spectrum disorder are observed in the majority of older children and adults. Most affected infants have significant but nonspecific features at birth such as neonatal hypotonia and feeding problems. Some affected individuals come to medical attention with respiratory or vision problems. Facial features may be mildly dysmorphic, but are nonspecific. To date, 18 individuals have been identified with WAC-related ID.
Developmental and epileptic encephalopathy 104
MedGen UID:
1823956
Concept ID:
C5774183
Disease or Syndrome
Developmental and epileptic encephalopathy-104 (DEE104) is an autosomal dominant disorder characterized by developmental delay in the first few months of life and drug-resistant focal and generalized tonic-clonic seizures (summary by Bott et al., 2021). For a general phenotypic description and a discussion of genetic heterogeneity of DEE, see 308350.
Tessadori-Van Haaften neurodevelopmental syndrome 3
MedGen UID:
1824083
Concept ID:
C5774310
Disease or Syndrome
Tessadori-Bicknell-van Haaften neurodevelopmental syndrome-3 (TEBIVANED3) is characterized by global developmental delay with poor overall growth, impaired intellectual development, and speech difficulties. More variable features include hypotonia, microcephaly, and dysmorphic facies. The severity and manifestations of the disorder are highly variable (Tessadori et al., 2022). For a discussion of genetic heterogeneity of Tessadori-Bicknell-van Haaften neurodevelopmental disorder, see TEBIVANED1 (619758).
Multiple mitochondrial dysfunctions syndrome 7
MedGen UID:
1841222
Concept ID:
C5830586
Disease or Syndrome
Mitochondrial dysfunctions syndrome-7 (MMDS7) is an autosomal recessive disorder characterized by a clinical spectrum ranging from neonatal fatal glycine encephalopathy to an attenuated phenotype of developmental delay, behavioral problems, limited epilepsy, and variable movement problems (Arribas-Carreira et al., 2023). For a general description and a discussion of genetic heterogeneity of multiple mitochondrial dysfunctions syndrome, see MMDS1 (605711).

Professional guidelines

PubMed

Smith HAB, Besunder JB, Betters KA, Johnson PN, Srinivasan V, Stormorken A, Farrington E, Golianu B, Godshall AJ, Acinelli L, Almgren C, Bailey CH, Boyd JM, Cisco MJ, Damian M, deAlmeida ML, Fehr J, Fenton KE, Gilliland F, Grant MJC, Howell J, Ruggles CA, Simone S, Su F, Sullivan JE, Tegtmeyer K, Traube C, Williams S, Berkenbosch JW
Pediatr Crit Care Med 2022 Feb 1;23(2):e74-e110. doi: 10.1097/PCC.0000000000002873. PMID: 35119438
Stollings JL, Kotfis K, Chanques G, Pun BT, Pandharipande PP, Ely EW
Intensive Care Med 2021 Oct;47(10):1089-1103. Epub 2021 Aug 16 doi: 10.1007/s00134-021-06503-1. PMID: 34401939Free PMC Article
Devlin JW, Skrobik Y, Gélinas C, Needham DM, Slooter AJC, Pandharipande PP, Watson PL, Weinhouse GL, Nunnally ME, Rochwerg B, Balas MC, van den Boogaard M, Bosma KJ, Brummel NE, Chanques G, Denehy L, Drouot X, Fraser GL, Harris JE, Joffe AM, Kho ME, Kress JP, Lanphere JA, McKinley S, Neufeld KJ, Pisani MA, Payen JF, Pun BT, Puntillo KA, Riker RR, Robinson BRH, Shehabi Y, Szumita PM, Winkelman C, Centofanti JE, Price C, Nikayin S, Misak CJ, Flood PD, Kiedrowski K, Alhazzani W
Crit Care Med 2018 Sep;46(9):e825-e873. doi: 10.1097/CCM.0000000000003299. PMID: 30113379

Recent clinical studies

Etiology

Sano M, Cummings J, Auer S, Bergh S, Fischer CE, Gerritsen D, Grossberg G, Ismail Z, Lanctôt K, Lapid MI, Mintzer J, Palm R, Rosenberg PB, Splaine M, Zhong K, Zhu CW
Int Psychogeriatr 2024 Apr;36(4):238-250. Epub 2023 Mar 7 doi: 10.1017/S1041610222001041. PMID: 36880250Free PMC Article
Crowley KE, Urben L, Hacobian G, Geiger KL
Clin Ther 2020 Apr;42(4):e65-e73. Epub 2020 Apr 6 doi: 10.1016/j.clinthera.2020.02.007. PMID: 32273047
Lee SJ, Sung TY
Korean J Anesthesiol 2020 Dec;73(6):471-485. Epub 2020 Mar 25 doi: 10.4097/kja.20097. PMID: 32209961Free PMC Article
Garriga M, Pacchiarotti I, Kasper S, Zeller SL, Allen MH, Vázquez G, Baldaçara L, San L, McAllister-Williams RH, Fountoulakis KN, Courtet P, Naber D, Chan EW, Fagiolini A, Möller HJ, Grunze H, Llorca PM, Jaffe RL, Yatham LN, Hidalgo-Mazzei D, Passamar M, Messer T, Bernardo M, Vieta E
World J Biol Psychiatry 2016;17(2):86-128. doi: 10.3109/15622975.2015.1132007. PMID: 26912127
Majić T, Gutzmann H, Heinz A, Lang UE, Rapp MA
Am J Geriatr Psychiatry 2013 Nov;21(11):1052-9. Epub 2013 Jul 3 doi: 10.1016/j.jagp.2013.03.004. PMID: 23831177

Diagnosis

Rahmani E, Lemelle TM, Samarbafzadeh E, Kablinger AS
J Head Trauma Rehabil 2021 Jul-Aug 01;36(4):E262-E283. doi: 10.1097/HTR.0000000000000656. PMID: 33656478
Lee SJ, Sung TY
Korean J Anesthesiol 2020 Dec;73(6):471-485. Epub 2020 Mar 25 doi: 10.4097/kja.20097. PMID: 32209961Free PMC Article
Deardorff WJ, Grossberg GT
Handb Clin Neurol 2019;165:5-32. doi: 10.1016/B978-0-444-64012-3.00002-2. PMID: 31727229
Rodriguez-Cabezas L, Clark C
Clin Obstet Gynecol 2018 Sep;61(3):615-627. doi: 10.1097/GRF.0000000000000377. PMID: 29794819Free PMC Article
Garriga M, Pacchiarotti I, Kasper S, Zeller SL, Allen MH, Vázquez G, Baldaçara L, San L, McAllister-Williams RH, Fountoulakis KN, Courtet P, Naber D, Chan EW, Fagiolini A, Möller HJ, Grunze H, Llorca PM, Jaffe RL, Yatham LN, Hidalgo-Mazzei D, Passamar M, Messer T, Bernardo M, Vieta E
World J Biol Psychiatry 2016;17(2):86-128. doi: 10.3109/15622975.2015.1132007. PMID: 26912127

Therapy

Chen H, Wang Y, Zhang M, Wang N, Li Y, Liu Y
Psychiatry Res 2022 Aug;314:114619. Epub 2022 May 10 doi: 10.1016/j.psychres.2022.114619. PMID: 35623240
Mühlbauer V, Möhler R, Dichter MN, Zuidema SU, Köpke S, Luijendijk HJ
Cochrane Database Syst Rev 2021 Dec 17;12(12):CD013304. doi: 10.1002/14651858.CD013304.pub2. PMID: 34918337Free PMC Article
Ball EL, Owen-Booth B, Gray A, Shenkin SD, Hewitt J, McCleery J
Cochrane Database Syst Rev 2020 Aug 19;8(8):CD003150. doi: 10.1002/14651858.CD003150.pub3. PMID: 32813272Free PMC Article
van der Steen JT, Smaling HJ, van der Wouden JC, Bruinsma MS, Scholten RJ, Vink AC
Cochrane Database Syst Rev 2018 Jul 23;7(7):CD003477. doi: 10.1002/14651858.CD003477.pub4. PMID: 30033623Free PMC Article
Garriga M, Pacchiarotti I, Kasper S, Zeller SL, Allen MH, Vázquez G, Baldaçara L, San L, McAllister-Williams RH, Fountoulakis KN, Courtet P, Naber D, Chan EW, Fagiolini A, Möller HJ, Grunze H, Llorca PM, Jaffe RL, Yatham LN, Hidalgo-Mazzei D, Passamar M, Messer T, Bernardo M, Vieta E
World J Biol Psychiatry 2016;17(2):86-128. doi: 10.3109/15622975.2015.1132007. PMID: 26912127

Prognosis

Wolak JP
Emerg Med Clin North Am 2021 May;39(2):307-322. doi: 10.1016/j.emc.2021.01.008. PMID: 33863461
Hui D, De La Rosa A, Wilson A, Nguyen T, Wu J, Delgado-Guay M, Azhar A, Arthur J, Epner D, Haider A, De La Cruz M, Heung Y, Tanco K, Dalal S, Reddy A, Williams J, Amin S, Armstrong TS, Breitbart W, Bruera E
Lancet Oncol 2020 Jul;21(7):989-998. Epub 2020 May 29 doi: 10.1016/S1470-2045(20)30307-7. PMID: 32479786Free PMC Article
Urits I, Peck J, Giacomazzi S, Patel R, Wolf J, Mathew D, Schwartz R, Kassem H, Urman RD, Kaye AD, Viswanath O
Adv Ther 2020 May;37(5):1897-1909. Epub 2020 Apr 9 doi: 10.1007/s12325-020-01317-x. PMID: 32274749
Resnick B, Boltz M, Galik E, Holmes S, Vigne E, Fix S, Zhu S
Pain Manag Nurs 2019 Jun;20(3):192-197. Epub 2019 May 10 doi: 10.1016/j.pmn.2019.02.008. PMID: 31080144Free PMC Article
Thwaites D, McCann S, Broderick P
J Palliat Med 2004 Aug;7(4):545-50. doi: 10.1089/jpm.2004.7.545. PMID: 15353098

Clinical prediction guides

Lee S, Sohn JY, Hwang IE, Lee HJ, Yoon S, Bahk JH, Kim BR
Br J Anaesth 2023 Apr;130(4):439-445. Epub 2023 Jan 23 doi: 10.1016/j.bja.2022.12.009. PMID: 36697272
Preskorn SH, Zeller S, Citrome L, Finman J, Goldberg JF, Fava M, Kakar R, De Vivo M, Yocca FD, Risinger R
JAMA 2022 Feb 22;327(8):727-736. doi: 10.1001/jama.2022.0799. PMID: 35191924Free PMC Article
Banerjee S, High J, Stirling S, Shepstone L, Swart AM, Telling T, Henderson C, Ballard C, Bentham P, Burns A, Farina N, Fox C, Francis P, Howard R, Knapp M, Leroi I, Livingston G, Nilforooshan R, Nurock S, O'Brien J, Price A, Thomas AJ, Tabet N
Lancet 2021 Oct 23;398(10310):1487-1497. doi: 10.1016/S0140-6736(21)01210-1. PMID: 34688369Free PMC Article
Hui D, De La Rosa A, Wilson A, Nguyen T, Wu J, Delgado-Guay M, Azhar A, Arthur J, Epner D, Haider A, De La Cruz M, Heung Y, Tanco K, Dalal S, Reddy A, Williams J, Amin S, Armstrong TS, Breitbart W, Bruera E
Lancet Oncol 2020 Jul;21(7):989-998. Epub 2020 May 29 doi: 10.1016/S1470-2045(20)30307-7. PMID: 32479786Free PMC Article
Cummings JL, Mega M, Gray K, Rosenberg-Thompson S, Carusi DA, Gornbein J
Neurology 1994 Dec;44(12):2308-14. doi: 10.1212/wnl.44.12.2308. PMID: 7991117

Recent systematic reviews

Silva EAD Junior, Medeiros WMB, Torro N, Sousa JMM, Almeida IBCM, Costa FBD, Pontes KM, Nunes ELG, Rosa MDD, Albuquerque KLGD
Trends Psychiatry Psychother 2022 Jun 13;44:e20200149. doi: 10.47626/2237-6089-2020-0149. PMID: 34043900Free PMC Article
Mühlbauer V, Möhler R, Dichter MN, Zuidema SU, Köpke S, Luijendijk HJ
Cochrane Database Syst Rev 2021 Dec 17;12(12):CD013304. doi: 10.1002/14651858.CD013304.pub2. PMID: 34918337Free PMC Article
Payne LE, Gagnon DJ, Riker RR, Seder DB, Glisic EK, Morris JG, Fraser GL
Crit Care 2017 Nov 14;21(1):276. doi: 10.1186/s13054-017-1856-1. PMID: 29137682Free PMC Article
Abraha I, Rimland JM, Trotta FM, Dell'Aquila G, Cruz-Jentoft A, Petrovic M, Gudmundsson A, Soiza R, O'Mahony D, Guaita A, Cherubini A
BMJ Open 2017 Mar 16;7(3):e012759. doi: 10.1136/bmjopen-2016-012759. PMID: 28302633Free PMC Article
Garriga M, Pacchiarotti I, Kasper S, Zeller SL, Allen MH, Vázquez G, Baldaçara L, San L, McAllister-Williams RH, Fountoulakis KN, Courtet P, Naber D, Chan EW, Fagiolini A, Möller HJ, Grunze H, Llorca PM, Jaffe RL, Yatham LN, Hidalgo-Mazzei D, Passamar M, Messer T, Bernardo M, Vieta E
World J Biol Psychiatry 2016;17(2):86-128. doi: 10.3109/15622975.2015.1132007. PMID: 26912127

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