METHODS: The present sample included 110 participants aged 20-60 years old. Participants were invited to provide their information on sociodemographic variables (age, gender, and educational level) and clinical characteristics (age at onset of depression and duration of illness) and to complete a series of cognitive performance measures including the Trail Making Tests A (psychomotor speed) and B (executive function), the Digit Symbol Substitution Test (attention), and the Auditory Verbal Learning Test (immediate free recall, acquisition phase, and delayed recall). The Mini International Neuropsychiatric Interview Version 6.0 was used to confirm the diagnosis of MDD and the Montgomery-Åsberg Depression Rating Scale was used to assess illness severity.
RESULTS: At the bivariate level, relations of age and educational level to all cognitive deficit domains were significant. At the multivariate level, only educational level and illness severity consistently and significantly predicted all cognitive deficits domains.
CONCLUSIONS: Therapeutic modalities should be individualised whilst considering the impacts of cognitive deficits in an attempt to prevent further deterioration in psychosocial functioning of MDD patients.KEY POINTSCognitive deficits are an elemental component of Major Depressive Disorder (MDD) persisting during a current major depressive episode or during remission, altering individuals' ability to process information and changes the way they perceive and interact with the environment.Cognitive deficits in MDD are evident among the upper-middle income groups in South-Eastern Asian countries warranting more local research as such deficits could lead to functional decline and work performance such as absenteeism and presenteeism.Therapeutic modalities should be individualised by taking the impacts of cognitive deficits into consideration to promote psychosocial functioning of MDD patients.
CASE REPORT: We report a case of paraparetic spectrum of GBS in a 53-year-old lady who presented with rapidly progressive acute flaccid paralysis involving both lower extremities with areflexia eight days after the first dose of Sinovac vaccine for SARS-CoV-2 in Malaysia. Cerebrospinal fluid (CSF) albuminocytological dissociation was seen and nerve conduction study (NCS) revealed sensory neuropathy. The diagnosis of GBS was made based on the Brighton criteria. Patient responded well to intravenous immunoglobulin (IVIG).
CONCLUSION: Though there is currently no convincing evidence of any causation between GBS and SARS- CoV-2 vaccination, clinicians should remain vigilant and consider GBS in the differential diagnosis for patient who presents with weakness with reduced or absent deep tendon reflex after vaccination against SARS-CoV-2.