He wrote that he had only encountered it four times in his career and gave brief descriptions of each case, listing three common traits:

The individual is tainted [by heredity] (hereditär belastete)
The subjects primary attraction is to children, rather than adults. The acts committed by the subject are typically not intercourse, but rather involve inappropriate touching or manipulating the child into performing an act on the subject.He mentions several cases of pedophilia among adult women (provided by another physician), and also considered the abuse of boys by homosexual men to be extremely rare. Further clarifying this point, he indicated that cases of adult men who have some medical or neurological disorder and abuse a male child are not true pedophilia and that, in his observation, victims of such men tended to be older and pubescent. He also lists pseudopaedophilia as a related condition wherein "individuals who have lost libido for the adult through masturbation and subsequently turn to children for the gratification of their sexual appetite" and claimed this is much more common.Austrian neurologist Sigmund Freud briefly wrote about the topic in his 1905 book Three Essays on the Theory of Sexuality in a section titled The Sexually immature and Animals as Sexual objects. He wrote that exclusive pedophilia was rare and only occasionally were prepubescent children exclusive objects.
Type 3
Patients with GEFS+ type 3 have mutations in the GABRG2 gene, which encodes the GABAA γ2 subunit (figure 2). The first mutation discovered in GABRG2 was K289M, in the extracellular region linking membrane-spanning domains M2 and M3. Oocytes injected with α1, β2, and γ2 subunits produce large GABA inducible currents whereas those injected with K289M mutant instead of wild-type subunits produce currents much smaller (about 10% of wild-type). This abnormal current is not the result of non-incorporation of mutant subunits since mutant containing receptors are still sensitive to benzodiazepines, a property for which functional γ subunits are required. Because of these results, it is believed that the GEFS+ phenotype in these individuals is a result of hyperexcitability.Concurrent with the previous mutation, a second group found a second mutation in GABRG2 associated with GEFS+. This mutation, R43Q, is located in the one of two benzodiazepine binding-sites located in the extracellular N-terminus. Benzodiazepines, such as Diazepam, potentiate GABA induced current. This potentiation is abolished in cells expressing the R43Q mutant subunit instead of the wild-type γ subunit. This mutation does not affect the subunits ability to coassemble into function receptors as it still confers resistance to GABA current blockade by zinc. As with the previous mutation, this mutation is expected to result in neuronal hyperexcitability.The final known GEFS+ type 3 mutation is a nonsense mutation, Q351X, located in the intracellular  region linking the third and fourth membrane spanning segments.