This kind of insecurity leads to overcompensation: compulsive formality, strict social observances and exaggerated displays of assurance.In 1950, Kurt Schneider described the "fanatic psychopaths" and divided them into two categories: the combative type that is very insistent about his false notions and actively quarrelsome, and the eccentric type that is passive, secretive, vulnerable to esoteric sects but nonetheless suspicious about others.The descriptions of Leonhard and Sheperd from the sixties describe paranoid people as overvaluing their abilities and attributing their failure to the ill-will of others; they also mention that their interpersonal relations are disturbed and they are in constant conflict with others.In 1975, Polatin described the paranoid personality as rigid, suspicious, watchful, self-centered and selfish, inwardly hypersensitive but emotionally undemonstrative. However, when there is a difference of opinion, the underlying mistrust, authoritarianism and rage burst through.In the 1980s, paranoid personality disorder received little attention, and when it did receive it, the focus was on its 
potential relationship to paranoid schizophrenia. The most significant contribution of this decade comes from Theodore Millon who divided the features of paranoid personality disorder to four categories:1) behavioral characteristics of vigilance, abrasive irritability and counterattack,
2) complaints indicating oversensitivity, social isolation and mistrust,
3) the dynamics of denying personal insecurities, attributing these to others and self-inflation through grandiose fantasies
4) coping style of detesting dependence and hostile distancing of oneself from others. Controversy
Due to repeated concerns of the validity of PPD and poor empirical evidence, it has been suggested that PPD be removed from the DSM.
Patients with paraneoplastic SPS generally lack other autoimmune issues but may have other paraneoplastic conditions.Stiff-limb syndrome is a variant of SPS. This syndrome develops into full SPS about 25% of the time. Stiffness and spasms are usually limited to the legs and hyperlordoisis generally does not occur. The stiffness begins in one limb and remains most prominent there. Sphincter and brainstem issues often occur with stiff-limb syndrome. Progressive encephalomyelitis with rigidity, another variant of the condition, includes symptoms of SPS with brainstem issues and autonomic disturbances. It involves polio-encephalomyelitis in the spine and brainstem. There is cerebellar and brainstem involvement. In some cases, the limbic system is affected, as well. Most patients have upper motoneuron issues and autonomic disturbances. Jerking SPS is another subtype of the condition. It begins like classical SPS and progresses for several years; up to 14 in some cases. It is then distinguished by the development of myoclonus as well as seizures and ataxia in some cases. Causes
Patients with SPS generally have high amounts of high glutamic acid decarboxylase antibody titers. About 80 percent of SPS patients have GAD antibodies, compared with about one percent of the general population. The overwhelming majority of people who have GAD antibodies do not contract SPS, indicating that systematic synthesis of the antibody is not the sole cause of SPS. GAD, a presynaptic autoantigen, is generally thought to play a key role in the condition, but exact details of the way that autoantibodies affect SPS patients are not known.