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To the Editor: Psychiatric disturbances, such as psychosis, have been often described during the course of multiple sclerosis (MS),1 but rarely at onset of the disease.2 In our work, we present two patients with psychotic disorders at onset of relapsing-remitting MS.
The first patient, a 26-year-old woman, was diagnosed with schizoaffective disorder after the acute appearance of auditory hallucinations and confusion; she was treated with antipsychotic drugs, without significant results. One year later, the patient developed weakness in the left leg and widespread paraesthesia. MR images showed demyelinating lesions in the white matter of the left temporal horn and in the dorsal spine. We made a diagnosis of MS,3 and she started glatiramer acetate treatment to prevent further relapses. To date, after 12 months from the beginning of treatment, the patient shows no relevant neurological and psychiatric alterations.
The second patient, a 30-year-old man, presented (2 years before our observation) with an episode characterized by psychomotor agitation with identity disturbances diagnosed as borderline personality disorder, and he started treatment with olanzapine without results. After a few months, he was referred to our department because of the development of lower-limb weakness and urge-incontinence. An MRI showed several lesions in the subcortical white matter and in the periventricular regions. All findings supported the diagnosis of MS, and the patient started beta-interferon treatment, with progressive clinical improvement, both in neurological and then in psychiatric alterations.
The exact percentage of psychiatric onset of MS is still unknown, but the number of MS patients with psychiatric onset may exceed 1%: in our experience, 2 among a cohort of 148 MS subjects had a psychiatric onset, about 1.3%. In our two cases, only the presence of abnormalities at the neurological examination induced clinicians to consider MS as cause of psychiatric disturbance.
Several reports highlight the association of psychotic symptoms with the presence of demyelinating lesions in the left temporal lobe. In our patients, one had temporal lesions, and the other had periventricular plaques, without significant relationship with the temporal lobe. In our opinion, it is not possible to establish a direct relationship between the sites of cerebral lesions and the psychiatric manifestations observed in MS.
After the psychiatric episode, both patients started long-term treatment with glatiramer acetate or beta-interferon. As reported in literature, glatiramer acetate also results in relief of affective disorders,4 whereas beta-interferon increases anxiety and depression.5 Nevertheless, in our patient, the administration of beta-interferon probably contributed to stabilizing the clinical picture.
Although studies on the prevalence of psychiatric onset of MS are few, we conclude that it may occur in more than 1% (in our experience, about 1.3%) and that, in previously healthy people with acute psychotic disorders, even the presence of the slightest neurological abnormality justifies a cranial MRI examination. Further studies are necessary to evaluate the factors that influence the development of psychiatric disorders in MS and the relationship between disease-modifying drugs and psychiatric disorders.
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