Non-pharmacologic treatments that have shown some degree of efficacy are electroconvulsive therapy (ECT), supportive psychotherapy, family and environment therapy, rehousing, risk management and treating underlying disorders in cases of secondary erotomania. ECT may provide temporary remission of delusional beliefs; antipsychotics help attenuate delusions and reduce agitation or associated dangerous behaviors, and SSRIs may be used to treat secondary depression. In delusional disorder there is some evidence that pimozide has superior efficacy compared with other antipsychotics. Psychosocial psychiatric interventions can enhance the quality of life through allowing some social functioning, and treating comorbid disorders is a priority for secondary erotomania. Family therapy, adjustment of socio-environmental factors, and replacing delusions with something positive may be beneficial to all. In most cases, harsh confrontation should be avoided. Structured risk assessment helps to manage risky behaviors in those individuals more likely to engage in actions that include violence, stalking, and crime. For particularly troublesome cases, neuroleptics and enforced separation may be moderately effective. History
Early references to the condition can be found in the work of Hippocrates, Freud (1911), G.G. de Clérambault (1942), Erasistratus, Plutarch and Galen. Parisian physician, Bartholomy Pardoux (1545-1611) covered the topics of nymphomania and erotomania. In 1623, erotomania was referred to in a treatise by Jacques Ferrand (Maladie damour ou Mélancolie érotique) and has been called "erotic paranoia" and "erotic self-referent delusion" until the common usage of the terms erotomania and de Clérambaults syndrome. In 1971 and 1977, M.V. Seeman referred to the disorder as "phantom lover syndrome" and "psychotic erotic transference reaction and delusional loving".
Diarrhea and vomiting are also relatively common, seen in at least 1% of people. Interactions
No interaction studies have been conducted. Because of its mechanism, tetrahydrobiopterin might interact with dihydrofolate reductase inhibitors like methotrexate and trimethoprim, and NO-enhancing drugs like nitroglycerin, molsidomine, minoxidil, and PDE5 inhibitors. Combination of tetrahydrobiopterin with levodopa can lead to increased excitability. Functions
Tetrahydrobiopterin has multiple roles in human biochemistry. The major one is to convert amino acids such as phenylalanine, tyrosine, and tryptophan to precursors of dopamine and serotonin, major monoamine neurotransmitters. It works as a cofactor, being required for an enzymes activity as a catalyst, mainly hydroxylases. Cofactor for tryptophan hydroxylases
Tetrahydrobiopterin is a cofactor for tryptophan hydroxylase (TPH) for the conversion of L-tryptophan (TRP) to 5-hydroxytryptophan (5-HTP). Cofactor for phenylalanine hydroxylase
Phenylalanine hydroxylase (PAH) catalyses the conversion of L-phenylalanine (PHE) to L-tyrosine (TYR). Therefore, a deficiency in tetrahydrobiopterin can cause a toxic buildup of L-phenylalanine, which manifests as the severe neurological issues seen in phenylketonuria. Cofactor for tyrosine hydroxylase
Tyrosine hydroxylase (TH) catalyses the conversion of L-tyrosine to L-DOPA (DOPA), which is the precursor for dopamine. Dopamine is a vital neurotransmitter, and is the precursor of norepinephrine and epinephrine. Thus, a deficiency of BH4 can lead to systemic deficiencies of dopamine, norepinephrine, and epinephrine. In fact, one of the primary conditions that can result from GTPCH-related BH4 deficiency is dopamine-responsive dystonia; currently, this condition is typically treated with carbidopa/levodopa, which directly restores dopamine levels within the brain.