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Biomedical subjects

C Larkin

Publications and source records attributed to C Larkin.

85 records · Page 5Linked to original sources
PubMed1988

'Early-onset schizophrenia' after teenage head injury. A case report with magnetic resonance imaging.

A 14-year-old youth sustained an injury to the left frontoparietal area, which was followed by evident change in personality and subsequently by an early-onset schizophrenia-like psychosis. Magnetic resonance imaging revealed ventricular dilatation, slightly more marked in the left hemisphere, and cortical atrophy. Some implications of this case for research on schizophrenia itself are discussed.

Adolescent↗
PubMed1983

Dietary intake, energy metabolism, and excretory losses of adult male germfree Wistar rats.

Adult germfree rats excreted 87% more calories with the feces than comparable conventional rats, but this loss was compensated by an 18% higher intake. As a result, energy utilization of germfree and conventional rats was similar (148 and 143 kcal/kg/day, respectively), although the germfree rat metabolized only 71.9% of its dietary intake, versus the conventional rat's 80%. Germfree rats consumed 33% more water than conventional rats. Both excreted approximately 33% of water intake via feces and urine, but the germfree rat excreted 56% of this with the feces, the conventional rat only 15%. Cecectomy of the germfree rat reduced water loss via the feces, but the total daily excretion of fecal dry matter remained comparable to that of the intact germfree rat. The increase in fecal dry matter excretion demonstrated by the germfree rat can be largely accounted for in terms of water-soluble organic material. The data imply that the lower oxygen consumption of the germfree rat is not coupled to a reduction in metabolized energy, but may be an anomaly linked to cecal stasis and enlargement.

Animals↗
PubMedDate not supplied

Schizophrenia: solving the puzzle.

BACKGROUND: Schizophrenia is a common mental illness with an incidence of 15 new cases per 100,000 population per year. AIM: To review evidence for current neurodevelopmental models of the aetiology of schizophrenia. METHODS: We performed a literature search using Medline and PsychINFO. We evaluated the relevance of each article and tracked other relevant articles through references. RESULTS: There is considerable evidence to support neurodevelopmental models of the aetiology of schizophrenia. One or more aetiological events occur between conception and birth that disturb central nervous system (CNS) development, leading to persisting alterations in brain structure and function. These early events, acting in concert with genetic loading and later influences or insults, predispose to the development of schizophrenia in early adulthood. CONCLUSIONS: There have been considerable advances in schizophrenia research over the past 20 years. Future study of Indices of neural development will help advance our understanding of this common, disabling mental illness.

Central Nervous System↗
PubMedDate not supplied

Compliance with neuroleptic medication in outpatients with schizophrenia; relationship to subjective response to neuroleptics; attitudes to medication and insight.

The relationship between compliance, subjective response to neuroleptics, attitudes to medication, and insight was assessed in a selected group of individuals with schizophrenia who were attending a catchment area outpatient psychiatric service. Regular compliers with medication reported a significantly better subjective response to neuroleptics and were more frequently prescribed depot medication compared with individuals who were irregularly compliant. There was no difference between regular and irregular compliers in terms of attitudes to medication or level of insight. There was a significant correlation between the measures of insight obtained using a self-report questionnaire (the Insight Scale [IS]) and a semistructured interview (the Scale for Assessment of Insight [SAI]).

Adult↗
PubMedDate not supplied

Course of psychopathology, cognition and neurobiological abnormality in schizophrenia: developmental origins and amelioration by antipsychotics?

It is argued that schizophrenia has origins in events occurring during the first or early second trimester that are reflected in minor physical anomalies and which may at least in part predispose to later obstetric complications. This neurodevelopmental basis underlies certain neuromotor and psychosocial abnormalities of infancy and childhood, which are the early manifestations of what will be reconceptualised later as negative symptoms and (particularly frontal) cognitive dysfunction, but gives rise to positive symptoms only on the maturation of other systems necessary for their expression. This later emergence of psychosis may reflect an active morbid process that is associated with increased accrual of negative symptoms and of general (but not frontal) cognitive impairment that may be ameliorated by effective antipsychotic treatment. The psychological or biological basis of this heuristic process is poorly understood. Contemporary re-appraisal of any impact of antipsychotics on the long-term course of schizophrenia must take into account what is known of the origins of the disease process with which such drugs might interact. Much recent work continues to indicate that very early events, during the embryonic/fetal period, are important in, if not fundamental to, the genesis of schizophrenia; i.e. that there is a neurodevelopmental basis to the disorder. The present article seeks to establish a time-line relating early intrauterine adversity and dysmorphogenesis, through the onset of psychosis, to the chronic phase of the illness over adulthood; from this time-line, a schema is elaborated for a beneficial impact of antipsychotics on the course of psychopathology, cognition and, less clearly, neurobiological abnormality.

Antipsychotic Agents↗
PubMedDate not supplied

Early cerebro-craniofacial dysmorphogenesis in schizophrenia: a lifetime trajectory model from neurodevelopmental basis to 'neuroprogressive' process.

Understanding the temporal origin(s) of schizophrenia, through specifying the earliest identifiable pathology, might indicate when to look for etiological factor(s), what their nature might be, and how course of illness might evolve from these origins. From this premise, earlier formulations are elaborated to offer a rigorously data-driven model that roots schizophrenia in cerebro-craniofacial dysmorphogenesis, particularly along the mid-line but involving other structures, over weeks 9/10 through 14/15 of gestation. However, a brain that has been compromised very early in fetal life is still subject to the normal endogenous programme of developmental, maturational and involutional processes on which a variety of exogenous biological insults and psychosocial stressors can impact adversely over later pregnancy, through infancy and childhood, to maturation and into old age, to sculpt brain structure and function; it should be emphasised that the effects of such endogenous programmes and exogenous insults on such an already developmentally-compromised brain may be different from their effects on a brain whose early fetal origins were unremarkable. From these early origins, a lifetime trajectory model for schizophrenia from developmental basis to 'neuroprogressive' process is constructed. Thereafter, consideration is given to what the model can explain, including cerebral asymmetry and homogeneity, what it cannot explain, what empirical findings would challenge or disprove the model, what cellular and molecular mechanisms might underpin the model, and what are its implications.

Brain↗
PubMedDate not supplied

Cell transplantation as an experimental treatment for Duchenne muscular dystrophy.

The feasibility, safety, and efficacy of myoblast transfer therapy (MIT) were assessed in an experimental lower body treatment (LBT) involving 32 Duchenne muscular dystrophy (DMD) boys aged 6-14 yr, half of whom were nonambulatory. Through 48 injections, five billion (55.6 x 10(6)/mL) normal myoblasts were transferred into 22 major muscles in both lower limbs, in 10 min with the subject under general anesthesia. Ten subjects received myoblasts cultured from satellite cells derived from 1-g fresh muscle biopsies of normal males aged 9-21 yr. Donor myoblasts for the remaining 22 boys were subcultured from reserves frozen 1 mo-1.5 yr ago. Only four donors were known to have identical histocompatibility with their recipients. All subjects took oral doses of the immunosuppressant cyclosporine (Cy), beginning at 2 days before MTT and lasting for 6 mo after MTT to facilitate donor cell survival. There was no evidence of an adverse reaction to MTT or Cy as determined by serial laboratory evaluations including electrolytes, creatinine, and urea. Objective functional tests using the KinCom Robotic Dynamometer measured the maximum isometric contractile forces of the ankle plantar flexors (AF), knee flexors (KF), and knee extensors (KE) before MTT and at 3, 6, and 9 mo after MTT. The AF, being distal muscles and less degenerative than the KE and the KF, showed no decrease in mean contractile force 3 mo after MTT, and progressive increases in force at 6 and 9 mo after MTT. At 9 mo after MTT, 60% of the 60 AF examined showed a mean increase of 50% in force; 28% showed no change; and only 12% showed a mean decrease in force of 29% when compared to the function of the same muscles before MTT. The KF, being proximal muscles and more degenerative, showed no change in function at 9 mo after MTT. The KE, being proximal and anti-gravitational, were most degenerative before MTT. They showed no statistically significant change in force at 3 mo after MTT but showed decreases at 6 and 9 mo after MTT. At 9 mo after MTT, 23% of the 60 KE examined showed a mean increase of 65% in force; 22% showed no change; and 55% showed a mean decrease of 24% in force. When results of all muscle groups (AF, KF, KE) were pooled, there was no change in force at 3, 6, or 9 mo after MTT vs. before MTT according to the Wilcoxon signed rank test.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗