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Biomedical subjects

M M Robertson

Publications and source records attributed to M M Robertson.

At least 37 records · Page 2Linked to original sources
PubMed1999

Outcome in refractory depression.

BACKGROUND: Failure to respond to first-line antidepressant treatment can occur in up to 40% of patients with depressive illness. A proven strategy for managing this refractory depression is lithium augmentation. The long-term outcome and optimal management of patients treated with lithium augmentation remains unclear. We describe a 4-8 year naturalistic follow-up of patients treated with lithium augmentation in two controlled studies of its efficacy in refractory depression. METHOD: Cases were followed up with personal interview where possible, and by telephone and general practitioner contact otherwise. Lifetime clinical status was ascertained using the Schedule for Affective Disorders and Schizophrenia-Lifetime (SADS-L). RESULTS: We obtained outcome data on 53 of the original eligible 76 patients. There was a good outcome in 38 (72%) patients. Good outcome was associated with a less endogenous nature of depression and an absence of previous hospitalisations. CONCLUSIONS: There do not seem to be any specific prognostic indicators of long-term outcome to lithium augmentation beyond those recognised to be relevant in the outcome of depression generally. LIMITATIONS: The conclusions are limited by incomplete follow-up of the total original sample and lack of objective illness and medication data for the intervening period.

Adult↗
PubMed1999

Depression and schizophrenia in epilepsy: social and biological risk factors.

BACKGROUND: In a retrospective study we investigated the role of social and biological risk factors for the development of major depression and schizophreniform psychoses in epilepsy. We tested the hypotheses that social risk factors are associated with depression and biological risk factors are associated with schizophreniform psychoses. METHOD: We studied 25 patients with epilepsy and paranoid-hallucinatory psychosis, 25 patients with epilepsy and major depression, and 50 non-psychiatric epilepsy patients (controls) with respect to biological and psychosocial variables. RESULTS: Schizophrenic patients had an earlier age of onset of epilepsy and a more severe epilepsy as characterised by history of status epilepticus, multiple seizure types and severity of seizures compared to non-psychiatric controls. Simple seizure symptoms were often vegetative and EEGs showed various abnormalities including temporal lobe discharges but no lateralisation to either side. With respect to antiepileptic drugs (AED) there were only few significant differences between groups: Polytherapy as well as treatment with phenytoin (DPH) was more frequent in psychotic patients as compared to non-psychiatric patients. Patients with psychoses were also characterized by a disturbed familial background, lack of interpersonal relationships, social dependency and professional failure. Depressive patients were significantly older than non-psychiatric controls and they suffered more frequently from focal epilepsies arising from the temporal lobe. They did not differ from controls with respect to severity of epilepsy. Treatment with valproate (VPA) was inversely linked with depression, suggesting that VPA may have prophylactic antidepressive properties in epilepsy patients. There were no psychosocial variables significantly linked with depression. CONCLUSIONS: In this study, patients with different forms of psychiatric complications in epilepsy could clearly be distinguished from controls. However, we could not confirm the simple hypothesis that there are biological predictors for schizophreniform psychoses and psychosocial predictors for major depression. Neurological and sociological variables seem linked with both, suggesting a multifactorial etiology.

Adult↗
PubMed1999

The prevalence of Gilles de la Tourette syndrome in children and adolescents with autism: a large scale study.

BACKGROUND: An earlier small-scale study of children with autism revealed that 8.1% of such patients were co-morbid for Gilles de la Tourette syndrome (GTS). The present study is a large scale test of whether this result replicates. METHOD: Four hundred and forty-seven pupils from nine schools for children and adolescents with autism were screened for the presence of motor and vocal tics. RESULTS: Subsequent family interviews confirmed the co-morbid diagnosis of definite GTS in 19 children, giving a prevalence rate of 4.3%. A further 10 children were diagnosed with probable GTS (2.2%). CONCLUSIONS: These results indicate that the rate of GTS in autism exceeds that expected by chance, and the combined rate (6.5%) is similar to the rates found in the smaller-scale study. Methodological considerations and alternative explanations for an increased prevalence are discussed.

Adolescent↗
PubMed1999

Depression in epilepsy: etiology, phenomenology, and treatment.

A history of depression or depressive symptomatology has been reported in up to two-thirds of patients with medically intractable epilepsy, whereas community studies have demonstrated affective disorder only in a quarter of these patients. Depression has been reported peri- and interictally. However, differentiation may be difficult in patients with frequent seizures. Most authors have found no correlation between depression and epilepsy variables. However, complex partial seizures, especially of temporal lobe origin, appear to be etiologic factors, particularly in men with left-sided foci. Depression is also more common in patients treated with polytherapy especially with barbiturates, phenytoin, and vigabatrin. Depression has also been described de novo after temporal lobectomy. Psychosocial factors also play a part, but underlying risk factors (e.g., genetic, endocrine and metabolic) may explain the increased rates of depression in people with epilepsy compared to those with other neurologic and chronic medical conditions. The depression appears to be endogenous. Patients tend to exhibit fewer neurotic traits and more psychotic symptoms such as paranoia, delusions, and persecutory auditory hallucinations. Treatment approaches include psychotherapy, rationalization of antiepileptic drug medication, antidepressant treatment, and ECT. The tricyclic and related antidepressants appear to be epileptogenic, especially in people at high risk (personal or family history of seizures, abnormal pretreatment EEG, brain damage, alcohol or substance abuse/withdrawal and concurrent use of CNS-active medication). Seizures tend to occur early in treatment or after dose increments, especially if rapidly titrated. There is little evidence that the newer antidepressants, e.g., selective serotonin reuptake inhibitors, moclobemide, venlafaxine, or nefazodone are more epileptogenic than placebo.

Adult↗
PubMed1998

Regulation of protein phosphatase 2A activity by caspase-3 during apoptosis.

Although the available evidence suggests that whereas the caspase family plays a major role in apoptosis, they are not the sole stimulators of death. A random yeast two-hybrid screen of a lymphocyte cDNA library (using caspase-3 as the bait) found an interaction between caspase-3 and the regulatory subunit Aalpha of protein phosphatase 2A. This protein was found to be a substrate for caspase-3, but not caspase-1, and could compete effectively against either a protein or synthetic peptide substrate. In Jurkat cells induced to undergo apoptosis with anti-Fas antibody, protein phosphatase 2A (PP2A) activity increased 4.5-fold after 6 h. By 12 h, the regulatory Aalpha subunit could no longer be detected in cell lysates. There was no change in the amount of the catalytic subunit. The effects on PP2A could be prevented by the caspase family inhibitors acetyl-Asp-Glu-Val-Asp (DEVD) aldehyde or Ac-DEVD fluoromethyl ketone. The mitogen-activated protein (MAP) kinase pathway is regulated by PP2A. At 12 h after the addition of anti-Fas antibody, a decrease in the amount of the phosphorylated forms of MAP kinase was observed. Again, this loss of activated MAP kinase could be prevented by the addition of DEVD-cho or DEVD-fmk. These data are consistent with a pathway whereby induction of apoptosis activates caspase-3. This enzyme then cleaves the regulatory Aalpha subunit of PP2A, increasing its activity. These data show that the activated PP2A will then effect a change in the phosphorylation state of the cell. These data provide a link between the caspases and signal transduction pathways.

Apoptosis↗
PubMed1998

Tic disorders: new developments in Tourette syndrome and related disorders.

The constellation of motor and vocal tics and certain of the other neuropsychiatric symptoms seen in Tourette syndrome are thought to have an organic basis, although the nature of the neurobiological lesion is uncertain. The syndrome is usually familial but the presumed genetic substrate has not been identified. A number of models currently under debate include a proposed autoimmune contribution.

Brain↗
PubMed1998

The prevalence of Tourette syndrome in a mainstream school population.

The aim of this study was to ascertain accurately the prevalence of Tourette syndrome (TS) in a mainstream school population. All year 9 pupils (aged 13 to 14 years) in a mainstream secondary school were investigated using a two-stage procedure. Standardized questionnaires were completed by parents, teachers, and pupils. Class observations were also carried out to identify tics. Those pupils identified as having tics underwent a semistructured interview to determine whether they had TS according to DSM-III-R criteria. Data were available from at least one source (parent, teacher, or self-reports) on 166 of the 167 pupils in the year. Five subjects were identified as having TS according to DSM-III-R criteria, yielding a prevalence estimate of 299 per 10,000 pupils in this age group. The results of this study suggest that TS in the community as a whole is more common and milder than those prevalence estimates and descriptions of the disorder based on TS encountered in secondary or tertiary health-care service settings.

Adolescent↗
PubMed1997

Neuroreceptor subunit genes and the genetic susceptibility to Gilles de la Tourette syndrome.

Segregation studies have shown that Gilles de la Tourette Syndrome (GTS) is probably transmitted as an autosomal dominant gene disorder and can therefore be studied by classical linkage analysis to identify susceptibility loci. Many neurotransmitter systems have been implicated in the etiology of GTS. Most recently the alpha-1 subunit of the glycine receptor etiologically responsible for hyperekplexia has been hypothesized as the cause of the susceptibility to GTS. Because of this and the high concentration of other neuroreceptor genes at 5q33-35, it was decided to study this region and the associated gene cluster on chromosome 4p12-16 in a large British kindred multiply affected with GTS and chronic motor tics. The genotypes of the microsatellite markers at these loci were determined by polymerase chain reaction. The allele data were analyzed using both parametric and nonparametric methods. Approximate multipoint maps were constructed across the regions of interest using FASTLINK. All of the lod scores produced were negative, showing no evidence of linkage to GTS in the family studied. The multipoint maps showed good exclusion across these regions. The glycine receptor gene responsible for hyperekplexia and the other neuroreceptor genes examined in this paper are not involved in the etiology of GTS in this large pedigree.

Alleles↗
PubMed1997

Obsessive compulsive symptoms in Gilles de la Tourette syndrome and obsessive compulsive disorder: differences by diagnosis and family history.

The distribution of obsessive compulsive symptoms was compared in 16 individuals with primary obsessive compulsive disorder (OCD) and 16 individuals with Gilles de la Tourette syndrome (GTS) and associated obsessive compulsive behaviors (OCB). The two groups showed significant differences in the distribution of OC symptomatology. Furthermore, those OCD probands who shared a similar symptom profile with GTS individuals all had a positive family history of OCD. All of the other OCD probands were isolated cases. Implications of this finding on the etiology and pathogenesis of the two disorders are discussed.

Adolescent↗
PubMed1997

Gilles de la Tourette's syndrome in special education schools: a United Kingdom study.

In order to determine the prevalence of tic disorders in children with severe school problems requiring a residential facility and comparison groups of children in regular day schools, we performed direct clinical examinations for the presence of tics and Gilles de la Tourette's syndrome (GTS) in 20 children from a residential school for emotional and behavioral difficulties (EBD); 25 children from a residential school for learning disabilities; 17 "problem" children (PC) (identified by teachers as having academic or behaviour problems) and 19 normal children (NC) selected at random (using random numbers) from a regular school. Of the EBD students, 65% were judged to have definite tics as compared with 24% of students with learning difficulties (P < 0.05), 6% of PC (P < 0.003) and none of the NC (P < 0.0006) group. Most of the affected students met diagnostic criteria for GTS. Our findings suggest that GTS is commonly associated with the need for special education and that this association is particularly robust for children with severe school problems. In these children, the presence of tics may be an indicator of an underlying dysfunction of neurological development.

Adolescent↗
PubMed1997

Tics associated with autistic and pervasive developmental disorders.

Coincident cases of Tourette syndrome and Pervasive Developmental Disorders increasingly have been reported in the literature. Coincident cases currently number around 90. A minority of cases have been associated with cases of Tourette syndrome and tics in other family members; this has led some authors to suggest that Tourette syndrome may be responsible for some of the genetic heterogeneity in Pervasive Developmental Disorders. The literature is reviewed, along with some aspects of the neurobiology of the two conditions with arguments for and against this hypothesis.

Autistic Disorder↗
PubMed1997

HMPAO SPET does not distinguish obsessive-compulsive and tic syndromes in families multiply affected with Gilles de la Tourette's syndrome.

BACKGROUND: Gilles de la Tourette's syndrome (GTS) is a familial neuropsychiatric disorder characterized by tics and obsessive-compulsive behaviours (OCB). Previous HMPAO SPET studies of subjects with GTS have shown hypoperfusion of striatal and frontal areas. Studies of patients with primary obsessive-compulsive disorder have shown, in contrast, hyperperfusion of similar areas. METHODS: Twenty subjects from five families affected by GTS, including individuals with OCB but no tics, were examined using HMPAO SPET. RESULTS: There were abnormalities of regional cerebral perfusion in individuals with GTS, OCB and tics. Hypoperfusion was in striatal, frontal and temporal areas. There was no hyperperfusion. CONCLUSIONS: Regional cerebral blood flow patterns in individuals with OCB in families affected by GTS are comparable to their relatives with GTS and differ from individuals with primary OCD in the absence of a family history of tic disorders.

Adolescent↗
PubMed1997

Seignot's paper on the treatment of Tourette's syndrome with haloperidol. Classic Text No. 31

The paper of Seignot in 1961 is the first clinical description of the use of haloperidol to treat the symptoms of Gilles de la Tourette syndrome (GTS). It is widely quoted in literature about GTS. However, it is not widely known that the single case involved had been subject to a frontal lobectomy prior to treatment with haloperidol. We present a translation of that paper and a discussion of its significance.

Haloperidol↗
PubMed1997

Personality disorder and psychopathology in Tourette's syndrome: a controlled study.

BACKGROUND: Some specialists associate a wide variety of psychopathologies with Tourette's syndrome (TS), while others suggest that there is no psychopathology specifically associated. Few controlled studies have been conducted to address this issue, and none has investigated personality disorder in TS. METHOD: Adults with TS and controls were evaluated using standardised psychiatric rating scales, including self-rated (STPCD) and clinician-rated (SCID-II) assessments of personality disorder, to investigate associations between personality disorder, other psychopathology and TS. RESULTS: Significantly more TS patients (25/39 (64%)) than controls (2/34 (6%)) had one or more personality disorders. TS subjects were also more likely to have more personality disorders. TS patients had significantly more depression, anxiety and obsessionality than controls. The SCID-II and STCPD were moderately well correlated. CONCLUSIONS: TS patients have a high prevalence of personality disorder and psychopathology when compared with controls. These results are the first to suggest a high level of personality disorder in a TS clinic population.

Adult↗