Humans ; Preventive Psychiatry ; Psychotic Disorders ; etiology ; prevention & control ; Risk Assessment

OBJECTIVE: To investigate the correlative factors for organic psychotic symptoms following traumatic brain injury (TBI). METHODS: In the current study, 391 subjects who had undergone forensic identification of the organic mental disorders due to TBI were included, both the demographic and post-traumatic information collected. The relevant data were statistically analyzed in those confirmed as organic psychotic syndrome according to Chinese Classification of Mental Disorders 3rd version (CCMD-3). RESULTS: Fifty-two subjects (13.3%) were identified as organic psychotic symptoms. The chi-square test showed that the detectable organic psychotic symptoms were associated with the marriage status, damage nature, injury severity and treatment, and the multivariate logistic regression analysis revealed good fitness of treatment and injury severity with the regression model (OR = 0.044, 95% CI: 0.017-0.114; OR = 2.145, 95% CI: 1.201-3.832, respectively). CONCLUSION The risks of organic psychotic symptoms following TBI can be involved in the alternative of craniotomy for the cases with trauma and moderate brain injury.
Brain Injuries/psychology* ; Humans ; Psychotic Disorders/etiology* ; Risk ; Syndrome

The clinical symptoms and signs of methamphetamine-associated psychosis (MAP) and schizophrenia are highly similar, but the situation is completely different when MAP and schizophrenia patients need to be assessed for criminal responsibility after they comitted a harmful behavior. Therefore, the distinction between the two psychoses is very important in forensic psychiatry. At present, the identification of these two psychoses is mainly dependent on the corresponding criteria such as the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) and the Chinese Classification of Mental Disorders Version 3 (CCMD-3). It's challenging to diagnose and distinguish between the two in practical cases due to their similar clinical symptoms and the lack of effective objective indexes. Different from the limitations of single omics, integrative omics intergrates data from multiple dimensions and has been extensively studied in the field of schizophrenia and has achieved some preliminary results. In view of the correlation between MAP and schizophrenia and the potential application value of integrative omics, this paper proposes an integrative omics strategy for MAP pathogenesis and forensic identification, aiming to improve the further understanding of the relationship between the two psychoses and the corresponding pathogenesis. It also provides references for the future exploration of integrative omics in forensic precise identification and effective monitoring and early warning methods.
Humans ; Methamphetamine/adverse effects* ; Psychoses, Substance-Induced/etiology* ; Psychotic Disorders/genetics* ; Schizophrenia/genetics* ; Diagnosis, Differential

We describe herein an unusual case of subacute thyroiditis presenting as acute psychosis. An 18-year-old male presented at the emergency department due to abnormal behavior, psychomotor agitation, sexual hyperactivity, and a paranoid mental state. Laboratory findings included an erythrocyte sedimentation rate of 36 mm/hr (normal range, 0 to 9), free T4 of 100.0 pmol/L (normal range, 11.5 to 22.7), and thyroid stimulating hormone of 0.018 mU/L (normal range, 0.35 to 5.5). A technetium-99m pertechnetate scan revealed homogeneously reduced activity in the thyroid gland. These results were compatible with subacute thyroiditis, and symptomatic conservative management was initiated. The patient's behavioral abnormalities and painful neck swelling gradually resolved and his thyroid function steadily recovered. Although a primary psychotic disorder should be strongly considered in the differential diagnosis, patients with an abrupt and unusual onset of psychotic symptoms should be screened for thyroid abnormalities. Furthermore, transient thyroiditis should be considered a possible underlying etiology, along with primary hyperthyroidism.
Acute Disease ; Adolescent ; Antipsychotic Agents/therapeutic use ; Humans ; Male ; Psychotic Disorders/diagnosis/drug therapy/*etiology ; Thyroiditis, Subacute/*complications/diagnosis/therapy ; Treatment Outcome

Methylenetetrahydrofolate reductase (MTHFR) deficiency is a rare autosomal recessive disorder. It is known that MTHFR deficiency may result in hyperhomocysteinemia, but MTHFR deficiency-induced schizophrenia has been rarely reported. Here we present the clinical course, biochemical and genetic characteristics of schizophrenia resulted from MTHFR deficiency in a school-age boy. He was 13 years old. He was admitted with a two-year history of fear, auditory hallucination, learning difficulty, sleeping problems, irascibility, drowsing and giggling. At admission, he had significantly elevated plasma and urine levels of total homocysteine, significantly decreased levels of folate in serum and cerebrospinal fluid, and a normal blood concentration of methionine. Further DNA sequencing analysis showed 665C>T homozygous mutations in the MTHFR gene. The patient was diagnosed with MTHFR deficiency-associated schizophrenia and treatment with calcium folinate, vitamin B12, vitamin B6, and betaine was initiated. After the treatment for 1 week, his plasma and urine levels of homocysteine were decreased to a normal range and the clinical symptoms were significantly improved. After 3 months of treatment, the patient returned to school. He is now living with normal school life. In summary, children with late-onset MTHFR deficiency and secondary cerebral folate deficiency may lead to schizophrenia. This rare condition can be early diagnosed through analyses of blood and urine total homocysteine, amino acids in blood and folate in blood and cerebral fluid and successfully treated with folinic acid, vitamin B6, vitamin B12 and betaine.
Adolescent ; Base Sequence ; Homocystinuria ; complications ; diagnosis ; drug therapy ; Humans ; Male ; Methylenetetrahydrofolate Reductase (NADPH2) ; deficiency ; Molecular Sequence Data ; Muscle Spasticity ; complications ; diagnosis ; drug therapy ; Psychotic Disorders ; complications ; diagnosis ; drug therapy ; Schizophrenia ; etiology

Niemann-Pick disease, type C (NP-C), is caused by NPC1 or NPC2 gene mutations. Progressive neurological, psychiatric, and visceral symptoms are characteristic. Here, we present cases of a brother (Case 1) and sister (Case 2) in their mid-20s with gait disturbance and psychosis. For the Case 1, neurological examination revealed dystonia, ataxia, vertical supranuclear-gaze palsy (VSGP), and global cognitive impairment. Case 2 showed milder, but similar symptoms, with cortical atrophy. Abdominal computed tomography showed hepatosplenomegaly in both cases. NPC1 gene sequencing revealed compound heterozygote for exon 9 (c.1552C>T [R518W]) and exon 18 (c.2780C>T [A927V]). Filipin-staining tests were also positive. When a young patient with ataxia or dystonia shows VSGP, NP-C should be considered.
Abdomen/diagnostic imaging ; Asian Continental Ancestry Group/genetics ; Carrier Proteins/genetics ; DNA Mutational Analysis ; Exons ; Female ; Gait Disorders, Neurologic/etiology ; Humans ; Male ; Membrane Glycoproteins/genetics ; Niemann-Pick Disease, Type C/*diagnosis/genetics ; Psychotic Disorders/etiology ; Republic of Korea ; Siblings ; Tomography, X-Ray Computed ; Young Adult