F. Ahmad

Bio: F. Ahmad is an academic researcher. The author has contributed to research in topics: Event (relativity) & Trait. The author has an hindex of 3, co-authored 6 publications receiving 296 citations.

Verbal self-monitoring and auditory verbal hallucinations in patients with schizophrenia.

Abstract: Background. Contemporary cognitive models of auditory verbal hallucinations propose that they arise through defective self-monitoring. We used a paradigm that engages verbal self-monitoring to investigate this theory in patients with schizophrenia. Methods. Ten patients with auditory verbal hallucinations and delusions (hallucinators), eight patients with delusions but no hallucinations (non-hallucinators), and 20 non-psychiatric control subjects were tested. Participants read single adjectives aloud, under the following randomized conditions: reading aloud; reading aloud with acoustic distortion of their own voice; reading aloud with alien feedback (someone else’s voice); and reading aloud with distorted alien feedback. Immediately after articulating each word, participants identified the source of the speech they heard (‘self’}‘other’}‘unsure’), via a button press. Response choice and reaction time were recorded. Results. When reading aloud with distorted feedback of their own voice, patients in both groups made more errors than controls; they either misidentified its source or were unsure. Hallucinators were particularly prone to misattributing their distorted voice to someone else, and were more likely to make errors when the words presented were derogatory. Both patient groups made faster decisions than controls about the source of distorted or alien speech, but faster responses were only associated with errors in the former condition. Conclusions. Impaired verbal self-monitoring was evident in both hallucinators and nonhallucinators. As both groups had delusions, the results suggest an association between delusions and impaired judgements about ambiguous sensory stimuli. The specific tendency of hallucinators to misattribute their distorted voice to someone else may reflect impaired awareness of internally generated verbal material.

Age-related changes in frontal and temporal lobe volumes in men: a magnetic resonance imaging study.

Abstract: Background Imaging and postmortem studies provide converging evidence that, beginning in adolescence, gray matter volume declines linearly until old age, while cerebrospinal fluid volumes are stable in adulthood (age 20-50 years). Given the fixed volume of the cranium in adulthood, it is surprising that most studies observe no white matter volume expansion after approximately age 20 years. We examined the effects of the aging process on the frontal and temporal lobes. Methods Seventy healthy adult men aged 19 to 76 years underwent magnetic resonance imaging. Coronal images focused on the frontal and temporal lobes were acquired using pulse sequences that maximized gray vs white matter contrast. The volumes of total frontal and temporal lobes as well as the gray and white matter subcomponents were evaluated. Results Age-related linear loss in gray matter volume in both frontal ( r = −0.62, P r = −0.48, P P P Conclusions The changes in white matter suggest that the adult brain is in a constant state of change roughly defined as periods of maturation continuing into the fifth decade of life followed by degeneration. Pathological states that interfere with such maturational processes could result in neurodevelopmental arrests in adulthood.

Structural Brain Imaging Evidence for Multiple Pathological Processes at Different Stages of Brain Development in Schizophrenia

Abstract: The underlying neurobiology of emerging psychotic disorders is not well understood. While there is evidence from structural imaging and other studies supporting the popular notion that schizophrenia arises as a consequence of an "early neurodevelopmental" lesion, more recent findings challenge this notion. Evidence, including our own data, suggests that dynamic brain changes occur during the earliest stages of a psychotic illness, including around the time of transition to illness. In this article we review the available longitudinal and relevant cross-sectional structural neuroimaging studies focusing on both the very early neurodevelopmental markers (pre- or perinatal origin) and the later markers (late neurodevelopmental) around the period of transition to illness. Based on our review of recent findings, we suggest that the onset of psychosis is a time of active brain changes, wherein, for a proportion of individuals, (i) an early (pre- and perinatal) neurodevelopmental lesion renders the brain vulnerable to anomalous late (particularly postpubertal) neurodevelopmental processes, as indicated by evidence for accelerated loss of gray matter and aberrant connectivity particularly in prefrontal regions; and (ii) these anomalous neurodevelopmental processes interact with other causative factors associated with the onset of psychosis (e.g., substance use, stress, and dysregulation of the hypothalamic-pituitary-adrenal axis function), which together have neuroprogressive sequelae involving medial temporal and orbital prefrontal regions, as suggested by imaging studies around transition to active illness. However, the pathological processes underlying such progressive changes during "late neurodevelopment" remain unclear but may reflect anomalies of synaptic plasticity, abnormal brain maturation, the adverse effects of stress, or other environmental factors. In this context, the features of schizophrenia, including the neuropsychological deficits and behavioral manifestations, can be understood as direct effects of these multiple pathological processes at various neurodevelopmental stages, including genetic and nongenetic etiological factors.

Ketamine-Induced Deficits in Auditory and Visual Context-Dependent Processing in Healthy Volunteers: Implications for Models of Cognitive Deficits in Schizophrenia

Abstract: Results: Ketamine significantly decreased the peak amplitudes of the MMN-to-pitch and MMN-to-duration deviants by 27% and 21%, respectively. It induced performance deficits in the AX-CPT characterized by decreased hit rates and specific increases of errors (BX errors), reflecting a failure to form and use transient memory traces of task relevant information. Conclusions: The NMDARs are critically involved in human MMN generation. Deficient MMN in schizophrenia thus suggests deficits in NMDAR-related neurotransmission. N-methyl-D-aspartate receptor dysfunction may also contribute to the impairment of patients with schizophrenia in forming and using transient memory traces in more complex tasks, such as the AX-CPT. Thus, NMDARrelated dysfunction may underlie deficits in transient memory at different levels of information processing in schizophrenia.