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Modern psychiatric nosologies separate catatonia along the lines of presumed etiology: bipolar, major depression, schizophrenia and due to a general medical condition. The presence of catatonia has always held diagnostic and prognostic value. Kahlbaum's description of catatonia includes careful documentation of phenomenology and the course of the illness. Since there were no effective treatments in his time, Kahlbaum was documenting the natural history of the illness.
A review of classic studies of the natural history of catatonia is that it is episodic, may have few other psychotic signs, may have periods of remission and may, in some cases, be associated with the disorganized subtype of schizophrenia. The literature of the past 100 years that support the validity of Dr. Kahlbaum’s description for a subset of patients with catatonia.
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Ludwig Karl Kahlbaum, was the physician and superintendent of the Reimer Sanitarium in Gorlitz, Germany. Dr. Kahlbaum has contributed a great deal to psychiatric classification.1 He is best known for his description of catatonia. He presented his first description of catatonia in Innsbruck in 1869 and later wrote his monograph entitled catatonia in 1873.2
Kahlbaum described catatonia in terms of motor abnormalities including mutism, negativism, stereotypies, catalepsy (waxy flexibility) and verbigeration.2 In addition, Kahlbaum described the natural course of the illness and the outcome in his series of patients.
Kraepelin certainly suggested that 'we may regard the catatonia of Kahlbaum as in the main a form, though peculiar, of dementia praecox.'3 However, in the next sentence he refines the position of catatonia : 'On the other hand "catatonic" morbid phenomena are undoubtedly also observed in many quite different morbid processes to a greater or less extent, so that its appearance alone does not justify the conclusion that catatonia, in the sense just indicated, is present.'3 In other words, Kraepelin clearly distinguished Kahlbaum's catatonia as a putative disease entity which he felt belonged to the group of dementia praecox, and catatonic symptoms or syndromes
('catatonic morbid phenomena') which may occur in different psychiatric disorders. Bleuler regarded catatonia as 'accessory manifestations of schizophrenia which 'may also appear in other types of illness'. The same notion was put by Bleuler more unequivocally: 'As is well known, catatonic symptoms do not solely occur in schizophrenia.' 4 In the subsequent paragraphs Bleuler gives a detailed account of individual catatonic symptoms occurring in healthy individuals and psychiatric disorders other than schizophrenia. In one of the most influential textbook of psychopathology of that era, Jaspers also mentioned that catatonic symptoms can be found in 'low-grade idiots', 'physically sick children' or in 'severe cases of encephalitis'5 The exclusive association between catatonia and schizophrenia was not even accepted by Kraepelin's pupils and closest allies as noted by Lange in an influential monograph on catatonic phenomena in manic illness.6
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Kahlbaum’s Monograph (1874)
"Catatonia is a brain disease with a cyclic, alternating course, in which the mental symptoms are, consecutively, melancholy, mania, stupor, confusion, and eventually dementia. One or more of theses symptoms may be absent from the complete series of psychic "symptom-complexes". In addition to the mental symptoms, locomotor neural processes with the general character of convulsions occur as typical symptoms." 2
Kahlbaum extrapolated the course from the disease catatonia (a symptom-complex) and based it upon the established illness syphilis -- generalized paralysis of the insane (GPI). For Kahlbaum, the natural course of the illness that he observed was affected by the lack of documented or available long-term follow-up. Furthermore, additional information may have been available to Kahlbaum which was not published in his monograph.
His patients were drawn from those sent to his sanitarium which may have created an ascertainment bias for more severe cases, and those with a longer duration of illness. His patients were a 19th century cohort. Syphilis and tuberculosis were have involved in a great number of cases and mortality was a significant factor in his studies of catatonia. It is also possible that cases of encephalitis lethargica occurred in 19th century prior to Von Economo’s first observations of this illness in 1916 in Vienna.8
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Catatonia and the Iowa 500
The Iowa 500 attempted to identify the natural history of psychiatric illness.13 Motor signs and other catatonic features were recorded in Iowa 500 charts. Catatonic signs were not very prevalent in the charts selected for affective disorders (depressive - 2.2%, bipolar - 11%). The highest prevalence of catatonic signs is in patients with schizophrenia (32%).13
Catatonic signs when present, held some prognostic value. Winokur and Tsuang separated hebephrenic-catatonic schizophrenia from paranoid schizophrenia.13 The hebephrenic-catatonic criteria include a large number of poor prognostic features in addition to motor symptoms. Pfohl and Winokur selected the charts of 52 hebephrenic-catatonic patients who required long term hospitalization from the Iowa 500.14 Each had year by year follow-up for 35 years. These patients had a low likelihood of full remission. Catatonic signs tended to disappear over time in this patient population. This subtype of schizophrenia appears to have more features of Hecker's description of hebephrenia than of Kahlbaum's description of catatonia.15
These Iowa 500 studies suggest that catatonia is a transient syndrome occurring in the course of hebephrenic schizophrenia. In this context, catatonia is associated with inappropriate affect, behavioral peculiarities, mild or transient motor phenomena and thought disorder. It has a deteriorating course and generally poor outcome.
The Iowa 500 studies retrospectively diagnosed patients schizophrenia of the hebephrenic-catatonic subtype.13
Both short-term and long-term follow-up was available for almost all cases. Treatment effect were present (ECT, antipsychotics and barbiturates). However, Winokur and others argued these do not substantially alter the natural course of schizophrenia, specifically. Such treatments, may however, may alter the expression of catatonia in this population.
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Hoch’s Benign Stupors (1921)
Dr. August A. Hoch is an interesting catatonia researcher. He was the Director for the State Psychiatric Institute, (Ward’s Island) in New York City from 1910 - 1917.9 During his career he collaborated with Dr. George H. Kirby on research into manic depressive illness and psychosis. Kirby is notable for being one of the first American researchers to demonstrate that catatonia occurred in manic-depressive illness (bipolar disorder).10
Dr. Hoch’s book “Benign Stupors” (1921) was published after his death.9 Dr. Hoch read Kahlbaum, Kraepelin and Blueler in German prior to the translations of their works into English.
In Benign Stupors, Hoch describes 25 cases of catatonia (stupor) with chapters on clinical features, diagnosis and treatment. He argued that cases 1 to 19 were catatonia due to manic-depressive illness, and cases 20 to 25 were malignant stupor, that is, stupor due to dementia praecox (schizophrenia). All cases were females were admitted to Ward’s Island. Almost all had follow-up by Dr. Hoch in the 1 up to 7 years following their index admission.
Hoch attempted to classify patients with "benign stupors" as a form of manic-depressive insanity with a more favorable outcome. Benign Stupors has been largely ignored, in spite of the fact that it provides an excellent description of catatonic signs, symptoms and course. This may be due to a follow-up study by Dr. Rachlin 25 years later.11 He located the patients or the charts of 13 of the available 18 patients from Hoch’s book. These were the patients that Hoch asserted had manic-depressive illness. However, Rachlin asserted that the concept of benign stupor was unreliable as many cases were most consistent with dementia praecox (schizophrenia).11
In preparation for this symposium, the author reviewed the cases from both the book and follow-up study with a focus on the course and outcome, independent of diagnosis. This provided an excellent opportunity to revisit Dr. Kahlbaum’s description of the course of the illness.2 Examined in this light, there are 6 cases of the 13 in which patients shifted from an episodic course to a chronic and deteriorating course with unfavorable outcome. Death occurred in several cases, usually pneumonia or tuberculosis associated with an institutional setting, so in these cases the natural course was truncated and conclusions could not be drawn.
Hoch's benign stupors when combined with Rachlin's follow-up provide both short-term and long-term follow-up in almost all of Hoch's 25 cases. His population is drawn from early 20th-century New York City. There are a great number of immigrants reflecting the composition of the working class of New York City at that time. Cases preceded the 1918 epoch of encephalitis lethargica. The greatest source bias in this series is that all his cases are women. There's a high incidence, 28% with post-partum onset of psychosis. However, the strength of this data is that it was collected before effective treatments were available.
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Catatonics Excluded From the Iowa 500
James Morrison, M.D. selected charts for the Iowa 500 and his studies of catatonia. From 1920 to 1971 there were nearly 20,000 patients admitted to the Iowa State Psychopathic Hospital. 2500 were diagnosed with schizophrenia and 10% (N=250) were diagnosed with catatonic state or catatonic schizophrenia. Over 90% (N=214) of these charts had follow-up data that could be blindly assessed.16
He found 40% (N=85) were recovered and compared them with those not recovered (N=129). Historical features associated with improvement included but were not limited to: 1) auditory hallucinations, 2) research diagnosis of schizophrenia, 3) acute onset, 4) disorientation, 5) previous episode with recovery, 6) age less than 20 years and 7) ECT (electroconvulsive therapy) administered. Motor signs had little predictive value; but two signs: 1) nudism and 2) stereotypies were associated with recovery.17
Those patients scored as recovered had not only returned to their premorbid personalities but were also asymptomatic and able to function in their old capacities. He noted that Kahlbaum's series of 27 patients, 41% recovered.2 In Kraepelin's series of dementia praecox, catatonic type, about 33% recovered.3 The outcome of the Non-500 catatonics is more favorable than non-catatonic schizophrenics. Table 2 shows the estimated recovery rate for catatonics from different studies.
Morrison further subdivided the 250 into retarded (N=110), excited (N=67) and mixed (N=73). The excited catatonics were more likely to be recovered (36%) and qualify for a research diagnosis of affective disorder (28%), predominately of the manic type (22%).18 Findings for the retarded type were less striking; 10% met research criteria for affective disorder (all depression) with 20% recovery. The mixed type fell in between with 15% meeting research criteria, evenly divided between mania and depression and a 24% recovery.
The diagnoses of both catatonic and hebephrenic schizophrenia had declined as a percentage in that hospital from the 1920s to the 1960s.16 The Morrison studies of catatonia (Iowa Non-500) and the Iowa 500 studies share the same ascertainment bias. Patients sent to the Iowa Psychopathic Hospital had to have a significant severity of illness and duration of the episode to necessitate traveling hundreds of miles over unfavorable road in order to be referred to this special state hospital. Treatment, most notably ECT, was observed to have an effect on the course of the illness. Both short-term and long-term follow-up were available. Morrison used the initial diagnosis catatonia to select cases. Consequently, good prognosis and poor prognosis cases were mixed together in his study populations.
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