An analysis of 17 catatonic patients diagnosed with neuroleptic malignant syndrome

This study was conducted to show that catatonia is a predisposing factor for neuroleptic malignant syndrome (NMS) and to review the nosological relationship between catatonia and NMS. Seventeen consecutive cases of NMS were analyzed prospectively with reference to clinical and investigative findings before and after exposure to a neuroleptic. The series comprised eight males and nine females, ranging in age from 18 years to 65 years. Prior to neuroleptic exposure, all patients exhibited features compatible with criteria for catatonia (mutism/excitement) according to the Diagnostic and Statistical Manual of Mental Disorders, Third Edition-Revised, (DSM-III-R). Following neuroleptic administration (single dose in nine cases), patients deteriorated into a febrile, rigid, and obtunded state accompanied by autonomic dysfunction and raised creatine phosphokinase levels. These features were consistent with a diagnosis of NMS. Neuroleptics were discontinued and supportive medical treatment instituted. Benzodiazepines were beneficial in eight cases in relieving stupor, but bromocriptine and dantrolene were generally ineffective. In all patients diagnosed with NMS in the authors' series, catatonia was an invariable prodromal state. It appears that the administration of a neuroleptic intensified the preexisting catatonic state and precipitated a malignant variant of the disorder, which is currently recognized as NMS. The authors, therefore, challenge the separate nosological status of NMS and catatonia and suggest that these syndromes are part of a unitary pathophysiological disorder.     

Progressive catatonia

We present the case of a young man with a diagnosis of a childhood-onset pervasive developmental disorder who developed a progressive neurologic deterioration with persistent catatonia and right hemiparesis. On his initial evaluation approximately three years after the onset of mutism, he manifested right hemiparesis and catalepsy. Two years later, although catalepsy had subsided, motor function had deteriorated so that he could not use his hands to feed or dress himself. Oral-facialbuccal dyskinesia manifested by blepharospasm and grimacing were present constantly during waking hours. Quantitative electroencephalography demonstrated markedly decreased amplitude, a finding associated with catatonia. Left sural nerve biopsy indicated large axon cylinder degeneration. Left deltoid biopsy demonstrated perimysial fibrosis and type II fiber predominance. Although magnetic resonance imaging of the head without contrast was normal, positron emission tomography indicated hypometabolism of the right cerebral and the right cerebellar hemispheres. The patient continues to deteriorate despite a course of 25 electroconvulsive treatments. He continues to manifest criteria for catatonia including motoric immobility, mutism, and peculiarities of voluntary movement such as prominent grimacing. We suspect an inherited neurodegenerative disorder. Since catatonia is a treatable condition frequently associated with medical and neurological diseases, examination for the features of catatonia must be included in the assessment of patients with progressive brain degeneration. This report is an attempt to clarify the traits of a serious variant of progressive brain degeneration.     

God-talk in therapeutic conversation

The article focuses on God-talk in the context of therapeutic conversations within a framework of psychodynamic and cognitive/narrative perspectives and develops a guide of five diagnostic questions for the critical analysis of God-stories as a tool in spiritual assessment. As a case-illustration, Anton Boisen's God-story is assessed with applications for Clinical Pastoral Education to learn from God-stories as "living human documents."     

What catatonia can tell us about "top-down modulation": a neuropsychiatric hypothesis

Differential diagnosis of motor symptoms, for example, akinesia, may be difficult in clinical neuropsychiatry. Symptoms may be either of neurologic origin, for example, Parkinson's disease, or of psychiatric origin, for example, catatonia, leading to a so-called "conflict of paradigms." Despite their different origins, symptoms may appear more or less clinically similar. Possibility of dissociation between origin and clinical appearance may reflect functional brain organisation in general, and cortical-cortical/subcortical relations in particular. It is therefore hypothesized that similarities and differences between Parkinson's disease and catatonia may be accounted for by distinct kinds of modulation between cortico-cortical and cortico-subcortical relations. Catatonia can be characterized by concurrent motor, emotional, and behavioural symptoms. The different symptoms may be accounted for by dysfunction in orbitofrontal-prefrontal/parietal cortical connectivity reflecting "horizontal modulation" of cortico-cortical relation. Furthermore, alteration in "top-down modulation" reflecting "vertical modulation" of caudate and other basal ganglia by GABA-ergic mediated orbitofrontal cortical deficits may account for motor symptoms in catatonia. Parkinson's disease, in contrast, can be characterized by predominant motor symptoms. Motor symptoms may be accounted for by altered "bottom-up modulation" between dopaminergic mediated deficits in striatum and premotor/motor cortex. Clinical similarities between Parkinson's disease and catatonia with respect to akinesia may be related with involvement of the basal ganglia in both disorders. Clinical differences with respect to emotional and behavioural symptoms may be related with involvement of different cortical areas, that is, orbitofrontal/parietal and premotor/motor cortex implying distinct kinds of modulation--"vertical" and "horizontal" modulation, respectively.     

"Scared stiff": catatonia as an evolutionary-based fear response

Catatonia, long viewed as a motor disorder, may be better understood as a fear response, akin to the animal defense strategy tonic immobility (after G. G. Gallup & J. D. Maser, 1977). This proposal, consistent with K. L. Kahlbaum's (1874/1973) original conception, is based on similarities between catatonia and tonic immobility ("death feint") as well as evidence that catatonia is associated with anxiety and agitated depression and responds dramatically to benzodiazepines. It is argued that catatonia originally derived from ancestral encounters with carnivores whose predatory instincts were triggered by movement but is now inappropriately expressed in very different modern threat situations. Found in a wide range of psychiatric and serious medical conditions, catatonia may represent a common "end state" response to feelings of imminent doom and can serve as a template to understand other psychiatric disorders.     

Brain imaging in catatonia: current findings and a pathophysiologic model

Karl Ludwig Kahlbaum originally described catatonia as a psychomotor disease that encompassed motor, affective, and behavioral symptoms. In the beginning of the 20th century, catatonia was considered to be the motoric manifestation of schizophrenia; therefore, neuropathologic research mostly focused on neuroanatomic substrates (ie, the basal ganglia underlying the generation of movements). Even though some alterations were found in basal ganglia, the findings in these subcortical structures are not consistent. Recently, there has been a reemergence of interest into researching catatonia. Brain imaging studies have shown major and specific alterations in a right hemispheric neural network that includes the medial and lateral orbitofrontal and posterior parietal cortex. This neural network may be abnormally modulated by altered functional interactions between gamma-aminobutyric acid (GABA)-ergic and glutamatergic transmission. This may account for the interrelationship among motor, emotional, and behavioral alterations observed in both clinical phenomenology and the subjective experiences of patients with catatonia. Such functional interrelationships should be explored in further detail in catatonia, which may also serve as a paradigmatic model for the investigation of psychomotor and brain function in general.     

Catatonia in affective disorder: new findings and a review of the literature

The historical development of the concept of catatonia in affective disorders and contemporary papers on this topic are reviewed. In addition, data from a current study on the frequency of catatonia in mixed mania are reported. Differences between catatonic and noncatatonic patients with mixed mania are presented and their relevance to clinical practice is discussed.     

The universal field hypothesis of catatonia and neuroleptic malignant syndrome

Catatonia and neuroleptic malignant syndrome (NMS) are uncommon disorders that can be life-threatening. Many researchers consider them as clinically divergent entities; however, they share similar and overlapping literature on causative agents, phenomenology, and treatment response. This hypothesis considers both disorders as a single entity that result from variable combinations of the following: 1) gamma-aminobutyric acid (GABA) hypoactivity at the GABAA receptor; 2) dopamine hypoactivity at the D2 receptor; 3) serotonin hyperactivity at the 5-HT1A receptor and hypoactivity at the 5-HT2A receptor; and 4) glutamate hypoactivity at the N-methyl-D-aspartate (NDMA) receptor. In this paper, evidence to support this hypothesis is limited to retrospective human studies of catatonia and NMS. The four components of the hypothesis are: 1) GABAA agonists have been shown to alleviate catatonia and NMS; 2) D2 antagonism is proportional to the relative likelihood of NMS and catatonia; 3) 5-HT1A agonism with 5-HT2A antagonism is implicated in catatonia and NMS; 4) NMDA receptor antagonists, such as phencyclidine and ketamine, reduce glutamate transmission. This hypothesis proposes that it is the interaction of these systems that prediposes, initiates, and maintains the twin syndromes of catatonia and NMS.     

Dyskinesias differentiate autistic disorder from catatonia

Autistic disorder and catatonia are neuropsychiatric syndromes defined by impairments in social interaction, communication, and restricted, stereotypical motor routines. Assessments of children with these disorders are typically restricted in scope by the patients' limited ability to comprehend directions. The authors performed systematic assessments of dyskinesias on six prepubertal boys with autistic disorder and mental retardation and on one adolescent male with catatonia to determine if this type of information could be routinely obtained. The boys with autistic disorder had more stereotypies and tics, a greater degree of akathisia and hyperactivity, and more compulsions than the adolescent with catatonia. Catatonia was associated with catalepsy and dystonic postures. The authors conclude that the diagnostic accuracy and specificity of neuropsychiatric syndromes may be enhanced by the systematic assessment of the dyskinesias associated with each condition.     

Anton Boisen revisited

Anton Boisen was both a psychologist of religion and a schizophrenic. His autobiography presents his case history but leaves many of his psychotic communications and experiences uninterpreted. This essay attempts to account for Boisen's most idiosyncratic psychotic products, drawing on theories of Jung and Bateson. Boisen and Jung both used experiences deriving from psychotic episodes to shape their subsequent life work. Boisen remained within liberal Protestantism, relinquishing his own crazy critique of Christianity developed during his mental illness. This critique is expressed through Boisen's notion of the Family of Four, a plan for world renewal that he himself never adequately interpreted.     

Mutism as permanent catatonic condition]

The history of a case of mutism, where the patient had been silent for more than twenty-five years, caused by the author to study and discuss this relatively infrequent catatonic symptom which is a type of schizophrenia, with frequent references being made to the results of psychiatric studies made by authors ranging from Kahlbaum to Leonhard. Permanent mutism as a possible phenomenal form was logically classified, by Leonhard, as a type of mannered catatonia.     

Exceptional musical performance in early childhood catatonia

Many years ago the author, jointly with a psychologist, described a patient who, in spite of her alleged idiocy, showed an exceptional musical capacity. However, in the meantime the author has recognized and described early childhood catatonics and, as a consequence of this new knowledge, he has to admit an error. Even according to our then findings it would have been identifiable that, as has been confirmed now by follow-up, the patient is suffering from catatonia, starting in infancy. The high musical performance, then arousing our greatest astonishment, is now explicable, for childhood schizophrenics do not develop general mental deficiency but only specific circumscribed deficits.     

Catatonic signs in medical and psychiatric catatonias

Patients with psychiatric catatonias vs those with medical catatonias may differ in catatonic phenomenology. To determine if these could be distinguished, the following methods were used: 1) a review of the literature; 2) a chart review; and 3) a prospective series. The literature review of 467 reports of medical catatonias yielded 240 cases that met research criteria. A chart review of 47 episodes of catatonia revealed a higher frequency of negativism in patients with medical catatonias. Prospective data obtained from rating scales revealed an increased frequency of echophenomena in patients with medical catatonias; however, no discriminate pattern of catatonic signs for medical catatonias arose. Overall, catatonic signs appear to share a similar distribution. These findings suggest that psychiatric and medical catatonias are indistinguishable based upon catatonic sign.     

Hereditary and psychosocial causes of schizophrenia

On the basis of the examination of patients with endogenic psychosis, indications were obtained that there are forms that mainly develop on a hereditary basis, and forms determined by psychosocial causes. In unsystematic schizophrenia the chief factors are hereditary, above all in periodic catatonia. On the other hand, there are a few indications of a hereditary genesis in systematic schizophrenia although it is just these forms that are distinguished by the severity of their course. By studying twins, cases of schizophrenia in infancy, and the circumstances of brothers and sisters, strong indications of psychosocial causes of systematic schizophrenia were found. Lack of contacts in the course of development appears to the determing factor. In motility psychosis, one of the cycloid psychoses, indications were found that excessive encouragement by other children can be a cause of overstrain and thus may be detrimental. The conclusions drawn are based on concrete findings obtained in a total of 1,114 cases and are for the most part statistically significant.     

“Emotionally, Soulfully, Spiritually ‘Free to Think and Act’: The Helen Flanders Dunbar (1902–59) Memorial Lecture on Psychosomatic Medicine and Pastoral Care”

This essay aims to stimulate rethinking about religious and medical healing and wholeness. While psychiatrist (Helen) Flanders Dunbar (1902–1959) is well known as a psychosomatic investigator and as Medical Director of the Council for Clinical Training, the initial home of Anton Boisen's groundbreaking movement for the clinical pastoral education of institutional chaplains and parish ministers, she is less appreciated as a theologically-trained scholar. This essay explores an earlier era's understanding of the spiritual and the more soulful components of healing and how Dunbar combined these to focus on helping all peoples become free to think and act. This essay was originally delivered as The Helen Flanders Dunbar Memorial Lecture on Psychosomatic Medicine and Pastoral Care at Columbia Presbyterian Center of the New York-Presbyterian Hospital, New York on November 2, 1999.     

Pattern of familial psychoses--systematic and unsystematic schizophrenia and cycloid psychoses]

604 cases were examined, 309 of which were systematic schizophrenics, 191 were unsystematic schizophrenics and 104 cycloid psychotics. With the systematic schizophrenics the average period spent in hospital amounted to 16.9 years, with the unsystematic schizophrenics 13.8 years, with the cycloid psychotics 8.2 years. The systematic schizophrenics were discharged from hospital on average 1.5 times, the unsystematic 2.3 times, the cycloid psychotics 4.1 times. Of the systematic schizophrenics, 37.5% were never discharged after their first admittance to hospital, of the unsystematic 25.7%, of the cycloid psychotics 9.6%. Bipolar fluctuations were detected in 1.6% of the systematic schizophrenics, 49.7% of the unsystematic and 78.8% of the cycloid psychotics. 15.9% of the systematic schizophrenics had occurrences of psychoses in their family compared to 50.8% of the unsystematic and 22.1% of the cycloid psychotics. The systematic schizophrenics had 17.5% of their family ill, the unsystematic 69.6%, the cycloid psychotics 25.0%. Of the parents of the systematic schizophrenics 2.3% were ill, of the parents of the unsystematic schizophrenics 11.6%, of the parents of the cycloid psychotics 5.0%. Of the brothers and sisters of the systematic schizophrenics 2.4% were ill, of the unsystematic schizophrenics 10.9%, of the cycloid psychotics 3.0%. These variations in the pattern and occurrence of psychoses in the family seem to prove that the three groups of endogenous psychoses are genetically separable. There are also differentiating features inside the groups. Periodic catatonia in particular is characterized by the great number of psychotics in the family.     

Tötungsdelinquenten im Normalvollzug unter besonderer Berücksichtigung psychiatrisch unauffälliger Mörder

We collected data on 121 cases of homicide and manslaughter in the normal penitentiary system and counted the cases of perpetrators with, and without, psychiatric diagnosis. About 30% of the sample consisted in perpetrators without any psychiatric diagnosis; in contrast, about 40% were diagnosed as personality disorder; some few cases (7%) were classified as alcoholism or polytoxicomania, respectively; and the rest (23%) were cases of both personality disorder and alcoholism/polytoxicomania. Perpetrators without psychiatric diagnosis differed in systematic ways from perpetrators with psychiatric diagnosis. The former committed their offenses more on victims in partnership and family, while perpetrators with psychiatric diagnosis frequently offended strangers. Perpetrators lacking a diagnosis used poison, and striking to dead, relatively more frequently while homicide and manslaughter by stabbing, shooting, or some combination thereof were committed mainly by perpetrators with psychiatric diagnosis. Diagnosed perpetrators had more frequently been previously convicted (nearly 70%). In sum we found a considerable percentage of perpetrators who lacked a psychiatric diagnosis. We argue that this group can properly be distinguished from perpetrators who have some psychiatric diagnosis.     

Prevalence of dual diagnosis in an institution for individuals who are developmentally handicapped

The prevalence of dual diagnosis (developmental handicap with accompanying mental illness) was examined in a population of 71 persons who are institutionalized and developmentally handicapped. The Reiss Screen for Maladaptive Behavior (Reiss, 1988) revealed that 69% of the popula- tion had a dual diagnosis. The incidence of dual diagnosis was not related to level of functioning, although the type of psychopathology varied considerably across levels of functioning. In contrast to findings from the Reiss Screen, previous psychiatric diagnosis indicated a much lower rate of dual diagnosis (26.8%), as did current psychiatric assessment. There was little agreement between the two psychiatric assessments, or between the Reiss Screen and the psychiatric assessments. The Reiss Screen appears to provide information of more practical value for community placement decisions than is provided by the psychiatric assessments. Limitations to the concept of ?dual diagnosis’? for characterizing the mental health needs of persons with a developmental handicap are discussed.     

Associations of a Sexually Transmitted Disease Diagnosis During a Relationship with Condom Use and Psychosocial Outcomes: (Short) Windows of Opportunity

Few studies have examined whether and how receiving an sexually transmitted disease (STD) diagnosis while in a romantic relationship relates to condom use and psychosocial sexual outcomes. Using dyadic data, we examined associations of a personal or a partner’s STD diagnosis during a relationship with condom use, monogamy intentions, condom intentions and attitudes, and STD susceptibility and communication. Because beliefs about how the STD was acquired may shape associations with behavior and cognitions, gender and suspecting that one’s partner had other sexual partners (i.e., partner concurrency) were examined as moderators. Participants were 592 individuals in 296 couples expecting a baby; 108 individuals had been diagnosed with an STD during the relationship. Personal STD diagnosis was unrelated to outcomes or was associated with increased risk. A partner’s diagnosis related to more positive condom intentions and attitudes. Among men who suspected concurrency, both a personal and a partner’s STD diagnosis were associated with less condom use. Receiving the STD diagnosis during pregnancy was associated with greater susceptibility and marginally greater condom use. Results suggest potential benefits of enhancing communication and encouraging joint risk reduction counseling among couples, engaging men more fully in preventive efforts, and capitalizing on the short window during which risk reduction occurs.     

Diagnosis of Fragile X Syndrome: A Qualitative Study of African American Families

Fragile X syndrome (FXS) is an inherited genetic condition with critical consequences to the proband and family members at all levels in the generations. Although evidence demonstrates that the rates of diagnosis for FXS are the same in all racial groups, age of diagnosis in African American children has been reported to occur later than in Caucasian children. Additionally, African American families are seriously under-represented in existing FXS research studies. As such, it is important to understand the possible disparities in the underlying factors to receiving a diagnosis in African American families with FXS. Herein, a qualitative approach was adopted to describe the overall FXS diagnosis experiences (pre-diagnosis, diagnosis, and post-diagnosis stages) of a convenience sample of 10 African American mothers. We identified three major findings among our participants: (1) FXS testing is not ordered immediately once a parent expresses concerns of developmental delays to the pediatricians, (2) the diagnosis is sometimes delivered in an insensitive manner with information often being outdated and unbalanced towards negative aspects, (3) communication issues among family members exists once the diagnosis is discovered. Although these qualitative data may not be representative of the whole group, these findings have significant implications for genetic counseling and our understanding in providing support and advocacy for African American families with FXS.