Abstract
Posttraumatic stress disorder (PTSD) is classified as an anxiety disorder in DSM-IV, and none of the DSM-IV diagnostic criteria refer to psychotic phenomena such as delusions or hallucinations. Yet some of the early literature did make reference to schizophrenia-like symptoms as an outcome of extreme trauma [1,2] and, recently, a number of reports [3–6] have discussed the emergence of psychotic symptoms in PTSD.
Traditionally, psychotic symptoms are confined to a limited range of syndromes in psychiatry: schizophrenia and related disorders, some mood disorders and organic disturbances. In general, prominent psychotic symptoms are not features of the anxiety disorders, the category to which PTSD has been assigned in DSM-IV. Thus, the emergence of frank psychotic symptoms in PTSD raises important nosological questions about the disorder. Recent literature on the topic is sparse, and the conclusions drawn remain controversial [7–9].
The aim of this paper therefore is to describe three patients with chronic PTSD who later developed psychotic features, and to discuss the nosological implications of these additional symptoms.
Case 1
A, a Chinese man in his forties, had been suffering from flashbacks, nightmares, poor concentration and hypervigilance for 2 years after he was physically assaulted by a group of men. At interview, he clearly fulfilled DSM-IV criteria for PTSD with a secondary major depression. As a consequence of his PTSD symptoms, his relationship with his wife and son deteriorated and he was unable to work. In addition, any exploration of his traumatic experience would lead to a worsening of his PTSD symptoms. Despite treatment using cognitive–behaviour therapy, supportive psychotherapy, several courses of different antidepressants, mood stabilisers and anxiolytics, his PTSD symptoms remained unchanged.
A year after commencing treatment, A developed a delusion that the men who had assaulted him were actually following him. He believed that they were planning to harm him and he even bought a knife to protect himself. On several occasions, he reported ‘seeing’ the assailants in his neighbourhood, but his wife refuted this. At interview, he showed evidence of persecutory delusions and visual hallucinations, but these symptoms were limited to experiences relating to the assailants involved in the assault. Various antipsychotic medications were prescribed including thioridazine (50 mg daily for 10 days), flupenthixol (20 mg depot monthly for 3 months) and risperidone (1 mg daily for 7 days). Each time he developed severe extrapyramidal side effects within 2 weeks of commencement, particularly akathisia, despite the use of low-dose antipsychotics and anticholinergic medication. The side effects were too severe for the patient to tolerate and medication had to be withdrawn. Consequently A was unwilling to try any other types of antipsychotics, but continued to be followed up. Unfortunately, both his PTSD and psychotic symptoms remained refractory to treatment.
Case 2
B, in her mid-twenties, had suffered from PTSD complicated by suicide attempts after she was gang-raped at the age of 18 years. In addition, she reported amnesic episodes that appeared consistent with fugue states: brief lapses in which she was unable to account for her time and how she came to be at various locations. The severity of her PTSD symptoms fluctuated over time, independent of the treatment she received (various antidepressants, anxiolytics, mood stabilisers as well as Eye Movement Desensitisation and Reprocessing and hypnosis).
After 2 years of follow up she began to report, for the first time, actually ‘seeing’ various members of the gang who had raped her. Whenever she approached the ‘assailants’, they seemed to ‘disappear’. At times, she reported ‘seeing’ the van that she was raped in driving past her. These visual hallucinations became more prominent whenever her PTSD symptoms worsened. She was prescribed various antipsychotic medications including thioridazine (10 mg daily for 14 days) and flupenthixol (20 mg depot monthly for 3 months), but each time she developed severe akathisia, despite using low doses and anticholinergic medication. In view of the severity of the side effects, the medication had to be withdrawn. Her PTSD symptoms became more tolerable when her treatment plan was changed to place more emphasis on supportive psychotherapy. Subsequently, she was able to return to work. She later decided to discontinue follow up, but at the time of termination, she continued to experience some PTSD symptoms and occasional visual hallucinations.
Case 3
K was a 49-year-old Bosnian refugee who had arrived in Australia 2 years previously. He had been psychologically healthy prior to the outbreak of the civil war in his country. During the war, he was drafted into the militia. At one point in the conflict, his group was completely surrounded by an enemy platoon, which included men he recognised from his own village. For 24 h, he and his comrades were forced to lie face down in the mud to evade detection, all the while being certain that they would be killed, and having to listen to the voices of the enemy calling out and threatening them. Miraculously, they evaded detection and they were rescued by compatriots the following day. K was in a state of ‘shock’ and was admitted to hospital for several months with a diagnosis of PTSD, for which he received medication.
His PTSD symptoms (insomnia, nightmares, flashbacks, avoidance, hyperarousal, irritability and poor concentration) persisted after his arrival in Australia, with the focus of his memories being on the single incident in which his group had been trapped in the mud. He was prescribed fluvoxamine (200 mg nocte) and given supportive counselling, with some improvement in his arousal and avoidance symptoms. After several months of treatment, however, he began to complain that assailants were following him, spying on him and intruding into his house. He could hear voices making threats outside his window. He claimed that on one occasion, they had entered his house at night and assaulted him. He acknowledged that his wife could not see the assailants. She attempted to reassure him that they were not ‘real’. On closer questioning, he reported that the intruders were members of the opposing militia from his village who had attempted to trap and kill him and his comrades. Risperidone (1 mg nocte for 14 days) was commenced with marginal relief only from his psychotic symptoms. When the dose was increased to 1 mg twice a day, K developed severe akathisia and he refused to continue taking any other antipsychotic medication. Both his PTSD and psychotic symptoms persisted without substantial improvement.
Discussion
All the cases discussed clearly met DSM-VI criteria for chronic PTSD before they developed persistent hallucinations and/or delusions. In each instance, the content of the psychotic symptoms was congruent with the traumatic experience. Phenomenologically, there was an absence of other positive or negative symptoms of schizophrenia. When low-dose antipsychotics were prescribed, all three patients developed severe extrapyramidal side effects. All insisted on ceasing the medication and refused any consideration of further antipsychotic agents. None of the patients were offered psychological interventions for their persistent positive symptoms of psychosis.
The evolution of hallucinations and delusions in patients with established PTSD raises important phenomenological and nosological questions. The delayed onset of psychotic symptoms precludes a diagnosis of an acute ‘reactive’ psychosis, which, by definition, should follow immediately after exposure to severe stress. The extension of PTSD to include paranoid symptoms may reflect a severity factor [4,7]. However, Sautter et al. [8] and Hamner et al. [9] concluded that the intensity of psychotic symptoms observed in this subgroup of PTSD sufferers was not attributable to the severity of PTSD symptoms. Even in proposed categories of complicated trauma reactions such as ‘complex’ PTSD [10,11], psychotic symptoms are not described.
The hallucinations or delusions in some cases of chronic PTSD may be extensions of dissociative phenomenon [2], but our patients were fully aware of their surroundings when they experienced psychotic symptoms and they retained complete memory for the experiences.
Schizophrenia and PTSD could coexist by chance, or the stress associated with the initial trauma, or with having PTSD itself, could precipitate schizophrenia in those who are constitutionally predisposed. Another possibility is that some patients suffer from a primary psychotic disorder that lowers their threshold for subsequent episodes of PTSD [12,13]. Our patients clearly did not conform to this pattern. It was noteworthy that all three patients developed severe extrapyramidal side effects at low dosages of antipsychotic medication. Other workers in the field [3–5] have noted a pattern of poor response to antipsychotics as well as striking neurological side effects in such patients. Although such a medication response pattern is somewhat atypical of schizophrenia, it cannot be regarded as strong evidence against that diagnosis. Also, our patients did not comply long enough with drug treatment to determine whether the core psychotic symptoms might respond to neuroleptic medication.
Much remains to be learnt about the phenomenology and psychopathology of PTSD. Although psychotic symptoms are unusual accompaniments to the disorder [14], their occurrence is being reported more frequently. Questions remain about the implications of these symptoms, but the impression derived from our cases is that the psychotic phenomena are closely related to, and appear to be elaborations, of underlying PTSD symptoms. As such, the nature of psychotic symptoms may be relevant to understanding the pathogenesis of the disorder. Hamner and Gold [15] reported altered levels of dopamine beta-hydroxylase which may differentiate psychotic from non-psychotic PTSD patients, suggesting that this may be a distinct subtype. Hence, the presence of such symptoms in some cases of PTSD raises questions about the boundaries of that disorder and whether it can always be confined nosologically to a subcategory of anxiety disorder.