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German Journal of Psychiatry

ISSN 1433-1055

Clinical Manifestations of Progressive Catatonia

James Robert Brašić1, 2, 3, David Zagzag4,5, S. Kowalik2,3, Leslie Prichep2,3, E. Roy John2,3,

Jacqueline Y. Barnett2,3, Brian Bronson2,3, Robert H. Nadrich2,3, Robert Cancro2,3,

Monte Buchsbaum6, and Carla Brathwaite7


1Department of Radiology and Radiological Science,

Johns Hopkins University School of Medicine, Baltimore, Maryland

2Department of Psychiatry, Bellevue Hospital Center, New York, New York

3Department of Psychiatry, New York University School of Medicine, New York, New York

4Department of Pathology, Bellevue Hospital Center, New York, New York

5Department of Pathology, New York University School of Medicine, New York, New York

6Department of Psychiatry, Mount Sinai School of Medicine, New York, New York

7Williams College, Williamstown, Massachusetts


 Corresponding author: J. R. Brašić, M.D., M. P. H., Division of Nuclear Medicine, Department of Radiology and Radiological Sciences, Johns Hopkins Outpatient Center, 601 North Caroline Street, Room 3245, Baltimore, Maryland 21287-0807, brasic@jhmi.edu


                                                                    Abstract

Background: Individuals with pervasive developmental disorders are vulnerable to the occurrence of catatonia and persistent functional deterioration. Objective: To facilitate the recognition of the clinical diagnosis of pervasive developmental disorder and catatonia, we describe the manifestations of a patient with a pervasive developmental disorder who exhibited progressive catatonia. Method: A young man with a pervasive developmental disorder who developed progressive catatonia at the age of 14 years was videotaped participating in a structured movement assessment battery over 9 sessions between 16 years 8 months and 19 years 9 months of age. Results: Mutism, social withdrawal, blepharospasm, grimacing, and inability to perform the activities of daily living progressively increase during the course of the illness. Conclusion: Pervasive developmental disorder and catatonia can be diagnosed and monitored in outpatient settings by the use of structured assessment protocols (German J Psychiatry 2000, 3:13-24)

Key Words: catatonia, blepharospasm, electroconvulsive therapy, grimacing, quantitative electroencephalography, tics

 

Introduction

Manifestations of the syndrome of catatonia include motoric immobility or stupor, excessive motor activity, extreme negativism or mutism, peculiarities of voluntary movement, and echolalia or echopraxia (American Psychiatric Association, 1994). Catatonia is associated with mood disorders, schizophrenia, and pervasive developmental disorders, as well as medical and neurological disorders (Brašić et al., 1999b; Cohen et al., 1999). Lorazepam and electroconvulsive therapy are effective treatments for catatonia (Bush et al., 1996). In this brief report of a young man with catatonia who exhibited a progressive neurobehavioral deterioration refractory to a course of twenty-five electroconvulsive therapies, we describe the clinical findings over the course of ten years with structured movement assessments, quantitative electroencephalogy, positron emission tomography, and neuropathology (Brašić et al., 1999a,b).

Methods

Subjects

CASE REPORT

Prenatal. His parents were 26 years old at the time of conception. While pregnant with the subject, his mother smoked a pack and a half of cigarettes daily and drank several cups of coffee daily, gained sixty pounds, had diabetes, toxemia, and hypertension, and was treated for pneumonia. After more than 24 hours of labor, delivery was induced under general anesthesia. He was the full-term product of a normal, uncomplicated vaginal delivery.

Postnatal. He had slight jaundice at birth treated with five days of phototherapy. He was a moderately active, colicky baby who was easy to comfort. He wore bars on his feet as an infant because they were turning out.

Illnesses. Until four of age he suffered from asthma. As a child he had bronchitis, frequent ear infections, and severe chronic constipation. At ten years of age he was hospitalized for four days for bowel obstruction.

Clinical Course. Although his development in the first three years of life was reportedly normal, he displayed abnormalities of speech and communication as well as an odd range of interests and activities consistent with a pervasive developmental disorder (American Psychiatric Association, 1994).  However, he does not meet the contemporary criteria for autistic disorder (Lord et al., 1994).

As a child he spoke slowly. He was teased at school due to his articulation deficits. Poor coordination including difficulties in gross and fine motor skills were present beginning in kindergarten. At ten years of age he was depressed when retained in fourth grade. This resolved when he was promoted to fifth grade. He read at grade level until eleven years of age. At eleven years of age his mathematics skills were delayed two years. From ten to fourteen years of age, psychological examinations yielded borderline global intellectual functioning.

When he was thirteen years old and in eighth grade, his teacher reportedly told him that he would not be promoted to high school. That afternoon he told his mother that he wanted to go to high school. That was the last time his mother heard him speak. His parents suspect sexual activity with his teacher; however, this was never confirmed.

At fourteen years and eight months of age, he attained a performance intelligence quotient of 63, indicating a mild range of mental retardation, on the Revised Wechsler Intelligence Scale for Children (WISC-R) (Wechsler 1974). The performance scale of the WISC-R (Wechsler 1974) alone was administered because he did not speak. Within the performance intelligence quotient, the highest score (average range) was found on a visual sequential reasoning task indicating the capacity for inner language (Racusin and Moss 1996).

At fourteen years and eleven months of age he was treated for a month with benztropine mesylate 1 mg twice daily and haloperidol 1 mg each morning and 3 mg at bedtime. This was discontinued due to lack of improvement.

At sixteen years and five months of age he exhibited frequent eye blinks. Glabellar, root, and snout reflexes were absent. Jaw jerk reflex was normal. Motor nerve conduction velocities, sensory nerve action potentials, and electromyography were normal.

At sixteen years and six months of age he exhibited blepharospasm, decreased saccades, and nystagmus, possibly rotatory. Kayser-Fleisher rings were absent.

At sixteen years and seven months of age quantitative electroencephalography demonstrated markedly diminished power (amplitude) in all wave bands (Young et al., 1996) (Figure 1). On the Peabody Picture Vocabulary Test-Revised (Dunn and Dunn 1981), his receptive vocabulary was within the first percentile rank (Racusin and Moss 1996).

At sixteen years and nine months of age snout reflex was present.

At seventeen years of age, his parents noticed right leg shaking, weakness of the right arm and leg, slower walking, and dragging the right leg.

At seventeen years and nine months of age, he first fell to his knees as he attempted to stand from sitting. With coaxing he walked hesitantly with stooped posture dragging his right leg. He had constant eye blink tics and facial grimaces.

At seventeen years and ten months of age he was started on 240 mg diltiazem by mouth daily at bedtime for high blood pressure. Radiographs of the spine showed kyphosis at C4 and C5, diminished height of the C5 and C6 vertebral bodies, and levoscoliosis at L5 with rotatory components.

At eighteen years of age his parents noted that he began to be unable to use his hands to feed himself.

At eighteen years and four months of age, he continued to take 240 mg diltiazem by mouth daily at bedtime for high blood pressure. Physical examination revealed stooped posture, decreased vertical and horizontal range of motion of both eyes, blepharospasm, grimacing, snout and glabellar reflexes, atrophy of the pectoral and hand muscles, and a 10x12 mm right epididymal cyst.

At eighteen years and five months of age, he began to require home attendants for bathing, feeding, and dressing.

At eighteen years and eight months of age, a biopsy of the left sural nerve showed degeneration of large axon cylinders (Figure 2) and a biopsy of the left deltoid muscle showed perimysial fibrosis and type II fiber predominance (Figure 3).

At nineteen years and eight months of age, renal ultrasound demonstrated a diffusely hyperechoic liver consistent with fatty infiltration. He received a course of twenty-five electroconvulsive treatments without improvement.

At nineteen years and ten months of age quantitative electroencephalography demonstrated an increase in delta and theta waves over all brain regions (Young et al., 1996) (Figure 4).

At twenty years and eleven months of age positron emission tomography of the brain was performed after the administration of 5 mCi of F-18 fluorodeoxyglucose. Decreased radiotracer localization was observed within the right temporal and parietal lobes. Mildly decreased localization was seen within the right frontal lobe and the right cerebellar hemisphere. Slightly decreased localization was present within the right basal ganglia (Young et al., 1996) (Figure 5).


Figure 1. Quantitative electroencephalography of a young man of sixteen years and seven months of age with progressive catatonia demonstrates markedly diminished power (amplitude) in all wave bands.

Topographic Z maps for absolute power (top row), relative power (second row), interhemispheric asymmetry (third row), and interhemispheric coherence (fourth row), in delta (first column), theta (second column), alpha (third column), and beta (fourth column) frequency bands. These maps represent the mean relative power difference between this subject and the normal reference group for his age expressed in standard deviation of the normal control group (not shown in the figure). Color coding is proportional to the mean Z-score for each group, in steps corresponding to those shown on the Z scale (range + 3.0). A Z score of + 1.96 is significant at the P < 0.05 level and of  + 2.57 at the P< 0.01 level. Black indicates no difference from age-expected normal values. Red indicates excesses over age-expected normal values. Blue indicated deficits under age-expected normal values.

N. B. The right side of the quantitative electroencephalography maps corresponds to the right side of the subject.

 

 

Figure 2.  Immunohistochemistry for neurofilament protein (NFP) of the left sural nerve of a young man with progressive catatonia. There is loss of axon cylinders (Immunoperoxidase, DAKO 2 F 11 antibody, ABC method, magnification x 100).

 

 

Figure 3. Muscle biopsy of the left deltoid muscle of a young man with progressive catatonia. There is a type II myofiber predominance. (ATPase stain, pH 10.4, magnification x 50).

 

 

 

Figure 4. Quantitative electroencephalography of a young man of nineteen years and ten months of age with progressive catatonia demonstrates an increase in delta and theta waves over all brain regions.

Topographic Z maps for absolute power (top row), relative power (second row), interhemispheric asymmetry (third row), and interhemispheric coherence (fourth row), in delta (first column), theta (second column), alpha (third column), and beta (fourth column) frequency bands. These maps represent the mean relative power difference between this subject and the normal reference group for his age expressed in standard deviation of the normal control group (not shown in the figure). Color coding is proportional to the mean Z-score for each group, in steps corresponding to those shown on the Z scale (range + 3.0). A Z score of + 1.96 is significant at the P < 0.05 level and of  + 2.57 at the P< 0.01 level. Black indicates no difference from age-expected normal values. Red indicates excesses over age-expected normal values. Blue indicated deficits under age-expected normal values.

N. B. The right side of the quantitative electroencephalography maps corresponds to the right side of the subject.

 

 

Figure 5. Positron emission tomography of the brain after the administration of 5 mCi of F-18 fluorodeoxyglucose to a young man of twenty years and eleven months of age with progressive catatonia. Decreased radiotracer localization is observed within the right temporal and parietal lobes. Mildly decreased localization is seen within the right frontal lobe and the right cerebellar hemisphere. Slightly decreased localization is present within the right basal ganglia

N. B. The right side of all figures for positron emission tomography corresponds to the left side of the subject.

 


Results

 The subject was evaluated in structured movement assessments employing a reliable protocol (Brašić et al., 1998) on nine occasions from sixteen years and eight months of age to nineteen years and two months of age. The videotapes of the original evaluations were rated in a nonblind fashion years after the original assessment by the child neuropsychiatrist who performed the original examination.

After viewing each videotaped session, the examiner completed rating scales for akathisia (Fleischhacker et al., 1989), attention deficit disorder (Leckman et al., 1988), obsessive compulsive disorder (Leckman et al., 1988), overall psychiatric functioning (Guy 1976, Pato and Pato 1991, Shaffer et al., 1985), parkinsonism (Paulson and Stern 1996), psychiatric symptomatology (Fish 1985, Guy 1976, Overall and Pfefferbaum, 1984), stereotypies (Campbell 1985), tics (Leckman et al., 1988, 1989), and other dyskinesias (Guy 1976, Simpson et al., 1979) (Table 1).

 

Table 1. Movement ratings of a young man with progressive catatonia 

Age   Years

16

17

17

17

17

18

18

19

19

Months

8

4

8

8.5

10

3

7

1

2

Medications

None

None

None

None

D

A, D

D

D

D

General dyskinesia

 

 

 

 

 

 

 

 

 

Abnormal Involuntary Movement Scale (Guy, 1976)

1

17

15

16

8

13

13

19

19

TDRS Face

20

21

31

28

27

28

31

27

28

TDRS Neck and trunk

8

8

11

11

8

11

14

17

13

TDRS Upper extremity

8

8

13

14

8

8

8

8

8

TDRS Lower extremity

8

8

8

8

8

8

8

8

8

TDRS Entire body

4

4

4

4

4

4

4

4

4

TDRS Total

48

49

67

65

55

55

65

64

61

Akathisia

 

 

 

 

 

 

 

 

 

HAS OI

0

0

0

0

0

0

0

0

0

HAS CGISA

1

1

1

1

1

1

1

1

1

HAS CGIGI

3

4

4

5

4

4

4

5

5

Parkinsonism

 

 

 

 

 

 

 

 

 

UPDRS MBM

3

4

4

4

4

4

4

4

4

UPDRS Activities of Daily Living

5

6

10

6

16

21

19

17

14

UPDRS Motor Examination

13

11

11

20

21

22

22

21

17

UPDRS Complications of Therapy

0

0

0

0

0

0

0

0

0

UPDRS MHYS

0

0

0

0

0

0

0

0

0

UPDRS SEADLS

76%

71%

71%

56%

10%

11%

10%

16%

19%

UPDRS Total

21

21

25

30

41

47

45

42

35

Stereotypies

 

 

 

 

 

 

 

 

 

Timed Stereotypies Rating Scale (Campbell, 1985)

31

20

50

51

40

81

44

60

59

Tics

 

 

 

 

 

 

 

 

 

TSCGIS

0

3

3

3

3

3

3

4

4

Yale Global Tic Severity Scale  (Leckman et al., 1989)

8

13

16

13

14

14

14

16

20

General psychiatric symptomatology

 

 

 

 

 

 

 

 

 

Brief Psychiatric Rating Scale (Guy, 1976)

22

25

29

27

31

26

27

28

29

BPRSC

22

20

30

33

30

30

33

32

35

Children’s Psychiatric Rating Scale A  (Fish, 1985)

32

41

44

57

47

53

50

50

52

Children’s Psychiatric Rating Scale B

9

6

12

12

11

9

10

10

18

Children’s Psychiatric  Rating Scale Total

41

47

56

69

58

62

60

60

70

Attention deficit disorder

 

 

 

 

 

 

 

 

 

ADDCGIS

0

0

0

0

0

0

0

0

0

Obsessive compulsive disorder

 

 

 

 

 

 

 

 

 

OCDCGIS

0

0

0

0

0

0

0

0

0

Overall psychiatric functioning

 

 

 

 

 

 

 

 

 

CGAS*

42

36

31

28

9

9

9

9

14

CGIRGE

4

4

5

6

4

4

4

6

6

CGISI

6

6

6

6

6

6

6

6

6

CGIGI

4

5

5

5

4

4

4

6

6

CGIEI

13

13

13

13

13

13

13

13

13

A = 250 mg amoxicillin by mouth daily

D = 240 mg diltiazem by mouth daily

Abbrevations:

ADDCGIS             Attention Deficit Disorder Clinical Global Impression Scale (Leckman et al., 1988)

BPRSC                 Brief Psychiatric Rating Scale for Children (Overall and Pfefferbaum, 1984)

CGAS                   Children’s Global Assessment Scale (Shaffer et al., 1985)*

CGIRGE               Clinical Global Improvement Rater Global Evaluation (Pato and Pato, 1991)

CGISA                  Clinical Global Impression Severity of Akathisia (Fleischhacker et al., 1989)

CGIEI                   Clinical Global Impressions Efficacy Index (Guy, 1976)

CGIGI                  Clinical Global Impression, Global Improvement (Fleischhacker et al., 1989; Guy, 1976)

CGISI                   Clinical Global Impressions, Severity of Illness (Guy, 1976)

HAS                     Hillside Akathisia Scale (Fleischhacker et al., 1989)

MBM                    Mentation, Behavior, and Mood (Paulson and Stern, 1996)

MHYS                  Modified Hoehn and Yahr Staging (Paulson and Stern, 1996)

OCDCGIS             Obsessive Compulsive Disorder Clinical Global Impression Scale (Leckman et al., 1988)

OI                         Objective Items (Fleischhacker et al., 1989)

SEADLS               Schwab and England Activities of Daily Living Scale (Paulson and Stern, 1996)

TDRS                   Tardive Dyskinesia Rating Scale (Simpson et al., 1979)

TSCGIS                Tourette Syndrome Clinical Global Impression Scale (Leckman et al., 1988)

UPDRS                 Unified Parkinson’s Disease Rating Scale (Paulson and Stern, 1996)

 

*On this scale only a higher score indicates better functioning.

Although the initial general dyskinesia ratings  (Guy 1976, Simpson et al., 1979) are normal, the scores increase over the years of assessment. The akathisia ratings  (Fleischhacker et al., 1989) reveal no evidence of akathisia during the videotaped sessions. The parkinsonism ratings show worsening of motor examinations and performance of activities of daily living throughout the ratings (Paulson and Stern 1996). This corresponds to the reports of the family that he became unable to feed, dress, and bathe and he began to require assistance for toilet activities. Both stereotypies (Campbell 1985) and tics (Leckman et al., 1988, 1989)  worsen throughout the course of the ratings. General psychiatric symptomatology scores (Fish 1985, Guy 1976, Overall and Pfefferbaum, 1984) and overall psychiatric functioning ratings (Guy 1976, Pato and Pato 1991, Shaffer et al., 1985) worsen throughout the course of the ratings. However, there is no evidence of attention deficit disorder (Leckman et al., 1988) or obsessive compulsive disorder  (Leckman et al., 1988) on any of the ratings (Table 1).

Discussion

We describe the clinical manifestations of catatonia followed by a progressive downhill course of neurologic deterioration in a young man. At sixteen years of age quantitative electroencephalography demonstrated decreased amplitudes in all frequencies. At eighteen years of age left sural nerve biopsy showed large axon cylinder degeneration and left deltoid muscle biopsy showed perimysial fibrosis and type II fiber predominance. At nineteen years of age after a course of twenty-five electroconvulsive treatments, quantitative electroencephalography revealed an increase in delta and theta waves over all brain regions. At twenty years of age positron emission tomography of the head demonstrated hypometabolism on the right side of the frontal, parietal, and temporal lobes, the basal ganglia, and the cerebellum.

On examination he exhibits constant tics in the form of bilateral eye blinking and, at other times, facial grimacing (Brašić et al., 1999a). Over the course of the illness, there are  increases in stereotypies, tics, and general dyskinesias in the face, neck, and trunk, and worsening in motor examination, psychiatric symptoms, overall functioning, and performance of activities of daily living.

We describe clinical features of a subject with progressive catatonia, a disorder of unknown etiology characterized by mutism, social withdrawal, prominent tics in the form of eye blinks and grimaces (Brašić et al., 1999a,b), and inability to perform the activities of daily living. Although this may represent tardive tics due to treatment with dopamine antagonists, we doubt this possibility because he received no more than 4 mg haloperidol daily for a month.

Quantitative electroencephalography initially at sixteen years and seven months of age demonstrated markedly diminished power (amplitude) in all wave bands (Figure 1), a finding suggesting diffuse dysfunction (Coppola and Hyde, 1995; Young et al., 1996) consistent with catatonia (Brašić et al., 1999b). However, three years and five months later at nineteen years and ten months of age, quantitative electroencephalography revealed an increase in delta and theta waves over all brain regions (Figure 4), an ominous sign consistent with deterioration of cerebral functioning (Coppola and Hyde, 1995; Young et al., 1996).

A year later at the age of twenty years and eleven months hypometabolism was demonstrated on positron emission tomography on the right side of the brain within the temporal, parietal, and frontal lobes, the right cerebellar hemisphere, and the right basal ganglia (Fig. 5). His right frontal hypometabolism (Figure 5) may be anatomically related to the catatonia and the negative symptoms which are prominently manifested in this subject (Schroder et al., 1996).

We suspect that the subject has an inherited neurodegenerative disorder (Chaves-Carballo, 1992), such as a forme fruste of an inherited neuronal storage disease (MacQueen et al., 1998) or a translated CAG expansion (Brice 1998).

An instructive feature of this subject is the meaningful use of a variety of rating scales developed for use with different psychiatric and neuropsychiatric disorders, i. e., schizophrenia and Parkinson’s disease. Many of the instruments are designed to be completed after an interview with the subject and the care givers. Since none of the authors have heard the subject talk in the ten years of treatment, a patient interview was omitted for this study. While the results of this subjects’s ratings therefore cannot be directly compared to those of patients with uncomplicated Tourette syndrome, for example, the ratings of the subject can be serially compared with other ratings of him because they were all conducted by a single clinician during the course of a few weeks. Several rating scales designed for other patient populations were remarkably well-suited for this subject. For example, with the Unified Parkinson’s Disease Rating Scale, the second and sixth sections to assess the activities of daily living, the third on the motor examination, and the total score (Paulson and Stern, 1996) well document the clinical decline manifested by this subject over the course of our study (Table 1). Additionally instruments designed to assess psychiatric functioning in children (Fish, 1985; Overall and Pfefferbaum, 1984; Shaffer et al., 1985) also well document objectively the deterioration in his functioning during the course of the study (Table 1). Despite the absence of a patient interview for this study, the rating scales designed for Tourette Syndrome (Leckman et al., 1988, 1989) were readily and effectively adapted and utilized for this markedly impaired subject (Table 1). Rating scales for tardive dyskinesia (Guy 1976; Simpson et al., 1979) were also well utilized for this subject although the prescribed patient interview was omitted (Table 1). These scales have items to sensitively quantitate the dyskinesias in the face, neck, and trunk, which are the areas affected in this subject.

There are several limitations to this report. All videotapes were reviewed and rated by a neurologist and child and adolescent psychiatrist who has been treating the subject for the course of the study. Therefore, the ratings were not conducted in a blind manner. Since only a single rater performed the ratings, reliability was not assessed. Future studies are needed to study the types of validity of this procedure, including construct, criterion-referenced, and predictive. Additionally, the reliability of the procedure including test-retest reliability, internal consistency, and alternate form reliability, must be evaluated (Brašić and Young, 1994). Also ratings need to be conducted in a blind manner on videotape segments presented in a random order by scientists who are unfamiliar with the subject and his treatment.

Acknowledgment

This research is supported by the Medical Fellows Program of the Consortium for Medical Education in Developmental Disabilities of the Office of Mental Retardation and Developmental Disabilities of the State of New York. This study is sponsored by the Department of Psychiatry of Bellevue Hospital Center and the New York University School of Medicine. The cooperation of Bellevue Hospital Center and the Health and Hospitals Corporation of the City of New York is gratefully acknowledged. An earlier version of this paper was presented at the Third International Scientific Symposium on Tourette Syndrome, Marriott World Trade Center Hotel, New York, New York, June 4-6, 1999.

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