The OPD is included in a group of personality and behavioural disorders - in the ICD-10 this is "Personality and behavioural disorders due to brain disease, damage and dysfunction", and in the ICD-11 this is "Secondary Mental or Behavioural Syndromes Associated with Disorders or Diseases Classified Elsewhere". This mental health disorder can be caused by disease, brain damages or dysfunctions in specific brain areas in frontal lobe. The most common reason for this profound change in personality is the traumatic brain injury. Children whose brain areas have been injured or damaged, may present with attention deficit hyperactivity disorder (ADHD), oppositional defiant disorder or OPD.OPD is most often caused by lesions in three brain areas of frontal lobe: traumatic brain injuries in orbitofrontal cortex, anterior cingulate cortex and dorsolateral prefrontal cortex. OPD may also be caused by lesions in other circumscribed brain areas.Another common feature of personality of patients with OPD is their dysfunctional and maladaptive behaviour that causes serious problems in these patients, because they face problems with pursuit and achievement of their goals. Patients with OPD express a feeling of unreasonable satisfaction and euphoria. Patients can show aggressive behaviour and these dysfunctions in behaviour can have effects on interpersonal relationships. One explanation of signs of anger and aggression is due to an inability to handle their impulses, this type of aggression being called "impulsive aggression". Diagnosis
ICD-11
In the ICD-11, the condition is called secondary personality change rather than organic personality disorder.
In the neuromuscular junction there is a vital pathway that maintains synaptic structure and results in the aggregation and localization of AChR on the postsynaptic folds. This pathway consists of agrin, muscle-specific tyrosine kinase (MuSK), acetylcholine receptors (AChRs) and the AChR-clustering protein rapsyn, encoded by the RAPSN gene. The vast majority of mutations causing CMS are found in the AChR subunits and rapsyn genes.Out of all mutations associated with CMS, more than half are mutations in one of the four genes encoding the adult acetylcholine receptor (AChR) subunits. Mutations of the AChR often result in endplate deficiency. Most of the mutations of the AChR are mutations of the CHRNE gene. The CHRNE gene codes for the epsilon subunit of the AChR. Most mutations are autosomal recessive loss-of-function mutations and as a result there is endplate AChR deficiency. CHRNE is associated with changing the kinetic properties of the AChR. One type of mutation of the epsilon subunit of the AChR introduces an Arginine into the binding site at the α/ε subunit interface of the receptor. The addition of a cationic Arg into the anionic environment of the AChR binding site greatly reduces the kinetic properties of the receptor. The result of the newly introduced Arg is a 30-fold reduction of agonist affinity, 75-fold reduction of gating efficiency, and an extremely weakened channel opening probability. This type of mutation results in an extremely fatal form of CMS.Another common underlying mechanism of CMS is the mutation of the rapsyn protein, coded by the RAPSN gene.