David Southall: David Southall is a British paediatrician who is an expert in international maternal and child hospital healthcare and in child protection including the diagnosis of the controversial Fabricated or Induced Illness (FII, also known as "Munchausen syndrome by proxy"), and who has performed significant research into sudden infant death syndrome.Personal injury
(1/41) Mothering to death.
Three families are described in which the healthy only child was, from early childhood, put to bed and treated as if ill, dependent, and incapable. This abnormal mothering continued for 28, 45, and 48 years, respectively, and the children died as disabled adults. In each case, the three mothers evaded medical, educational, and social services. The origins of their behaviour are examined, and the links with more common forms of separation anxiety, school refusal, and perceived and factitious illness are discussed. (+info)
(2/41) Hypoglycemia in adults.
Hypoglycemia is a clinical and biological syndrome, caused by an abnormal decrease in plasma glucose levels to below 0.55 g/l (3.0 mmol/l). Hypoglycemia is responsible for non-specific signs and symptoms which should be noted in a particular pathological context, and for secretion of counterregulatory hormones (mainly glucagon and catecholamines). Difficulty in identifying the etiology is variable, based upon history and physical examination, and hormonal investigations or imaging procedures, according to the results. Drug-related hypoglycemia is the most frequent observed cause (mainly in insulin-treated diabetic patients, but many drugs may be involved), followed par toxicity (alcohol mainly). Tumor-induced hypoglycemia is secondary to inappropriate insulin secretion by a beta-cell pancreatic tumor (insulinoma), and, rarely to an extrapancreatic mesenchymal large tumor secreting IGF-II. Hypoglycemia is present in other diseases, such as hormonal deficiencies, hepatic, or renal failure, or acute cardiac insufficiency. Multifactorial hypoglycemia seems to be underdiagnosed, mainly in hospitalized, underfed older patients with severe disease or sepsis. Autoimmune hypoglycemia is rare, due to insulin or insulin-receptor autoantibodies. Reactive hypoglycemia is observed after gastrectomy, but true primitive hypoglycemia appears to be rare, with false excess diagnosis in the majority of the cases. (+info)
(3/41) Instrumental psychosis: the Good Soldier Svejk syndrome.
The possession of severe mental illness, mainly schizophrenia and affective psychosis, may be perceived in positive terms. We have identified a group of patients, most of them with a history of previous psychotic disorder, who present with deliberately created symptoms and behaviour, and who are defined as having instrumental psychosis. Because most such patients have had a psychotic disorder in the past the symptoms are very like those of a real psychosis. A parallel is drawn with the fictional anti-hero of the Czech nation, the Good Soldier Svejk, who demonstrated both real and instrumental psychosis. A rating scale, the 'pseudopsychosis inventory', was devised to identify the main components of this disorder and was applied in 15 consecutive patients presenting with putative psychotic disorders in whom assessment could be made by two raters within five days. The inter-rater reliability of the items of the scale was good (intra-class correlation coefficient 0.68). An epidemiological study with this scale in 45 patients with a putative psychotic disorder suggested the presence of instrumental psychosis in 2. (+info)
(4/41) A case of thyroid storm due to thyrotoxicosis factitia.
We describe a case of thyroid storm due to thyrotoxicosis factitia, which was caused by the ingestion of excessive quantities of exogenous thyroid hormone for the purpose of reducing weight. An 18-year-old female was admitted to the hospital 24 hours after taking up to 50 tablets of synthyroid (1 tablet of synthyroid : levothyroxine 100 microg). Because of her stuporous mental state and acute respiratory failure, she was intubated and treated in the intensive care unit. After reviewing her history carefully and examining plasma thyroid hormone levels, we diagnosed this case as a thyroid storm due to thyrotoxicosis factitia. Her thyroid function test revealed that T3 was 305 ng/dL, T4 was 24.9 microg/dl, FT4 was 7.7 ng/dL, TSH was 0.05 micro IU/mL and TBG was 12.84 microg/mL (normal range: 11.3 - 28.9). TSH receptor antibody, antimicrosomal antibody, and antithyroglobulin antibody were negative. She was recovered by treatment, namely, steroid and propranolol, and was discharged 8 days after admission. Thyroid storm due to thyrotoxicosis factitia caused by the ingestion of excessive thyroid hormone is rarely reported worldwide. Therefore, we now report a case of thyroid storm that resulted from thyrotoxicosis factitia caused by the ingestion of a massive amount of thyroid hormone over a period of 6 months. (+info)
(5/41) Regional cerebral blood flow abnormalities in depressed patients with cognitive impairment.
Depression with cognitive impairment, so called depressive pseudodementia, is commonly mistaken for a neurodegenerative dementia. Using positron emission tomography (PET) derived measures of regional cerebral blood flow (rCBF) a cohort of 33 patients with major depression was studied. Ten patients displayed significant and reversible cognitive impairment. The patterns of rCBF of these patients were compared with a cohort of equally depressed non-cognitively impaired depressed patients. In the depressed cognitively impaired patients a profile of rCBF abnormalities was identified consisting of decreases in the left anterior medial prefrontal cortex and increases in the cerebellar vermis. These changes were additional to those seen in depression alone and are distinct from those described in neurodegenerative dementia. The cognitive impairment seen in a proportion of depressed patients would seem to be associated with dysfunction of neural systems distinct from those implicated in depression alone or the neurodegenerative dementias. (+info)
(6/41) The construct validity of the Lees-Haley Fake Bad Scale. Does this scale measure somatic malingering and feigned emotional distress?
The Fake Bad Scale (FBS [Psychol. Rep. 68 (1991) 203]) was created from MMPI-2 items to assess faking of physical complaints among personal injury claimants. Little psychometric information is available on the measure. This study was conducted to investigate the psychometric characteristics of the FBS using MMPI-2 profiles from six settings: Psychiatric Inpatient (N=6731); Correctional Facility (N=2897); Chronic Pain Program (N=4408); General Medical (N=5080); Veteran's Administration Hospital Inpatient (N=901); and Personal Injury Litigation (N=157). Most correlations of the FBS and raw scores on the MMPI-2 were positive with correlations among the validity scales being lower than correlations among the clinical and content scales. The FBS was most strongly correlated with raw scores on Hs, D, Hy, HEA, and DEP. When the more conservative cutoff of 26 was used, the FBS classified 2.4-30.6% of individuals as malingerers. The highest malingering classification was for the women's personal injury sample (37.9%) while the lowest was among male prison inmates (2.3%). Compared to men, in most samples, almost twice as many women were classified as malingerers. The results indicate that the FBS is more likely to measure general maladjustment and somatic complaints rather than malingering. The rate of false positives produced by the scale is unacceptably high, especially in psychiatric settings. The scale is likely to classify an unacceptably large number of individuals who are experiencing genuine psychological distress as malingerers. It is recommended that the FBS not be used in clinical settings nor should it be used during disability evaluations to determine malingering. (+info)
(7/41) Behavioural interventions in the rehabilitation of acute v. chronic non-organic (conversion/factitious) motor disorders.
BACKGROUND: Repeated case series have documented the effectiveness of multidisciplinary in-patient behavioural treatment for conversion disorders. However, in the absence of controlled research, treatment success could be attributed to providing patients with a face-saving opportunity to get better. AIMS: The present study contrasts two behavioural treatments to elucidate the factors underlying successful in-patient rehabilitation of this population. METHOD: Thirty-nine patients underwent a standard behavioural programme. Using a crossover design, patients who did not improve underwent a strategic-behavioural treatment in which they and their families were told that full recovery constituted proof of an organic aetiology whereas failure to recover was definitive proof of a psychiatric aetiology. RESULTS: Chart review indicated that the standard behavioural treatment was effective for 8/9 'acute' patients but only for 1/28 'chronic' patients. Of the 21 patients with chronic motor disorder who then under went the strategic-behavioural intervention, 13 were symptom-free at discharge. CONCLUSIONS: The strategic intervention was superior to standard behavioural treatment for patients with chronic motor disorder. Treatment components previously deemed critical for the effectiveness of behavioural treatment may be unnecessary. (+info)
(8/41) Meningeal derived cerebrospinal fluid proteins in different forms of dementia: is a meningopathy involved in normal pressure hydrocephalus?
OBJECTIVES: In animal models and in vitro studies leptomeninges have been shown to be the origin of neurotrophic substances that support the survival and growth of neuronal cells. Because dementia is associated with neuronal loss, we investigated whether leptomeningeal dysfunction may be involved in the pathogenesis of dementia disorders. METHODS: We analysed the cerebrospinal fluid (CSF) concentrations of the leptomeningeal derived beta trace protein, beta2 microglobulin, and cystatin C. RESULTS: There was a statistically significant difference of the CSF beta trace protein levels among different groups. Patients with idiopathic normal pressure hydrocephalus (NPH) (17.5 (SD 4.3) mg/l) showed significantly lower CSF beta trace protein levels than patients with Alzheimer's disease (23.8 (6.2) mg/l), depression (24.2 (7.3) mg/l), and normal controls (25.3 (4.9) mg/l). To patients with vascular dementia (20.1 (5.6) mg/l) and frontotemporal dementia (21.9 (7.0) mg/l), the difference was not significant. There was no significant difference regarding the CSF and serum concentrations of beta2 microglobulin or cystatin C among the different groups. CONCLUSIONS: We conclude that leptomeningeal dysfunction may be involved in certain types of dementia such as NPH and that reduced CSF beta trace protein levels in patients with NPH may aid in differentiating this difficult to diagnose disorder from other syndromes such as Alzheimer's disease. (+info)