“…Mood disturbance, including both depression and mania, is the most common formal neuropsychiatric illness [63-67]. Psychosis, delusional states and catatonia, while less frequent in WD, can be extremely disabling [56,57,60,61,68]. Schizophrenia-like symptoms were reported to be present in up to 10% of patients [63], but were less prevalent in one case series (2.4%) [69].…”
ObjectiveIt is important for psychiatrists to be aware of certain inborn errors of metabolism (IEMs) as these rare disorders can present as psychosis, and because definitive treatments may be available for treating the underlying metabolic cause. A systematic review was conducted to examine IEMs that often present with schizophrenia-like symptoms.Data sourcesPublished literature on MEDLINE was assessed regarding diseases of homocysteine metabolism (DHM; cystathionine beta-synthase deficiency [CbS-D] and homocysteinemia due to methyltetrahydrofolate reductase deficiency [MTHFR-D]), urea cycle disorders (UCD), acute porphyria (POR), Wilson disease (WD), cerebrotendinous-xanthomatosis (CTX) and Niemann-Pick disease type C (NP-C).Study selectionCase reports, case series or reviews with original data regarding psychiatric manifestations and cognitive impairment published between January 1967 and June 2012 were included based on a standardized four-step selection process.Data extractionAll selected articles were evaluated for descriptions of psychiatric signs (type, severity, natural history and treatment) in addition to key disease features.ResultsA total of 611 records were identified. Information from CbS-D (n = 2), MTHFR-D (n = 3), UCD (n = 8), POR (n = 12), WD (n = 11), CTX (n = 14) and NP-C publications (n = 9) were evaluated. Six non-systematic literature review publications were also included. In general, published reports did not provide explicit descriptions of psychiatric symptoms. The literature search findings are presented with a didactic perspective, showing key features for each disease and psychiatric signs that should trigger psychiatrists to suspect that psychotic symptoms may be secondary to an IEM.ConclusionIEMs with a psychiatric presentation and a lack of, or sub-clinical, neurological signs are rare, but should be considered in patients with atypical psychiatric symptoms.
“…Mood disturbance, including both depression and mania, is the most common formal neuropsychiatric illness [63-67]. Psychosis, delusional states and catatonia, while less frequent in WD, can be extremely disabling [56,57,60,61,68]. Schizophrenia-like symptoms were reported to be present in up to 10% of patients [63], but were less prevalent in one case series (2.4%) [69].…”
ObjectiveIt is important for psychiatrists to be aware of certain inborn errors of metabolism (IEMs) as these rare disorders can present as psychosis, and because definitive treatments may be available for treating the underlying metabolic cause. A systematic review was conducted to examine IEMs that often present with schizophrenia-like symptoms.Data sourcesPublished literature on MEDLINE was assessed regarding diseases of homocysteine metabolism (DHM; cystathionine beta-synthase deficiency [CbS-D] and homocysteinemia due to methyltetrahydrofolate reductase deficiency [MTHFR-D]), urea cycle disorders (UCD), acute porphyria (POR), Wilson disease (WD), cerebrotendinous-xanthomatosis (CTX) and Niemann-Pick disease type C (NP-C).Study selectionCase reports, case series or reviews with original data regarding psychiatric manifestations and cognitive impairment published between January 1967 and June 2012 were included based on a standardized four-step selection process.Data extractionAll selected articles were evaluated for descriptions of psychiatric signs (type, severity, natural history and treatment) in addition to key disease features.ResultsA total of 611 records were identified. Information from CbS-D (n = 2), MTHFR-D (n = 3), UCD (n = 8), POR (n = 12), WD (n = 11), CTX (n = 14) and NP-C publications (n = 9) were evaluated. Six non-systematic literature review publications were also included. In general, published reports did not provide explicit descriptions of psychiatric symptoms. The literature search findings are presented with a didactic perspective, showing key features for each disease and psychiatric signs that should trigger psychiatrists to suspect that psychotic symptoms may be secondary to an IEM.ConclusionIEMs with a psychiatric presentation and a lack of, or sub-clinical, neurological signs are rare, but should be considered in patients with atypical psychiatric symptoms.
“…Although fluoxetine may facilitate stress-induced 5-HT release within the locus coeruleus (Singewald et al 1997), there is evidence for an inhibitory rather than excitatory action of 5-HT on the activity of locus coeruleus neurons (e.g. Renaud et al 1975;Haddjeri et al 1997, Mateo et al 2000Szabo and Blier 2001; for review, see Singewald and Philippu 1998), suggesting that the facilitation of airjetinduced locus coeruleus activity by fluoxetine is not due to a local 5-HT effect. Similarly, although low abundance of 5-HT 2C receptor mRNA (Pompeiano et al 1994;Wright et al 1995) and binding (Singewald et al 1999) are found in the locus coeruleus, it is not likely that the activation of these receptors plays a predominant role since systemic, but not local administration of 5-HT2 receptor ligands, has been shown to affect the activity and reactivity of locus coeruleus neurons (Gorea et al 1991;Chiang and Aston-Jones 1993; for review, see Singewald and Philippu 1998;Harro and Oreland 2001).…”
Taken together, the results indicate that the anxiogenic-like effect as well as the facilitated neuronal reactivity induced by acute fluoxetine in the airjet model is mediated primarily by activation of 5-HT2C receptors.
“…Nevertheless, the experimental conditions in mice have not been subjected to extensive investigation; thus, mice appear to be more sensitive than rats to systematically administered clonidine (Porsolt et al 1979;de Graaf et al 1985). Clonidine is known to alter 5-HT transmission in vitro (Starke and Montel 1973;GSthert and Huth 1980;Maura et al 1982) and in vivo (Svensson et al 1975;Dresse and Scuvte-Moreau 1986); however, 5-HT has been suggested to either enhance (Trulson and Henderson 1985) or to attenuate (Renaud et al 1975) noradrenergic (NA) neuron activity.…”
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In the mouse forced-swimming model, dose-dependent reversal of immobility was induced by the alpha-agonist clonidine given IP 30 min before testing. In addition, three preferential inhibitors of 5-HT uptake (citalopram, indalpine and fluvoxamine) had similar activity in the dose range 8-16 mg/kg as did the 5-HT1 agonist 8-OH-DPAT (1-4 mg/kg). Pretreatment with alpha-methyl-paratyrosine (100 mg/kg) did not prevent clonidine (1 mg/kg) action, suggesting that there was mediation by alpha post-junctional receptors. The effect of clonidine was unaltered by prazosin (2 mg/kg) and reversed by yohimbine (4 mg/kg) and 5-MeODMT (1 mg/kg), whereas it was potentiated by reserpine (2.5 mg/kg), methysergide (2 mg/kg) and ketanserin (8 mg/kg). Moreover, an ineffective dose of clonidine (0.06 mg/kg at 45 min pre-testing) made active subthreshold doses of various antidepressants (given at 30 min pre-testing): imipramine (4 mg/kg), amitriptyline (1 mg/kg), maprotiline (8 mg/kg), citalopram (2 mg/kg), indalpine, fluvoxamine and mianserin (4 mg/kg), viloxazine (2 mg/kg). Similar interactions were found with iprindole and nialamide (32 mg/kg), which were inactive alone up to 64 mg/kg, and 8-OH-DPAT (0.5 mg/kg) but not with major and minor tranquillizers. It is suggested that one effect of antidepressants might be the triggering of different relationships between alpha-2 and 5-HT mechanisms.
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