- Email: [email protected]
Citalopram for post-stroke pathological crying
20 Bel EH, Zwinderman AH, Timmers MC, Dijkman JH, Sterk PJ. the protective effect of a beta2 agonist against excessive airway narrowing in response to bronchoconstrictor stimuli in asthma and chronic obstructive disease. Thorax 1991; 46: 9-14. 21 Larsson K, Martinsson A, Hjemdhal P. Influence of &bgr; adrenergic receptor function during terbutaline treatment on allergen sensitivity and bronchodilator response to terbutaline in asthmatic subjects. Chest 1992; 101: 953-60. 22 Wong CS, Wahedna I, Pavord ID, Tattersfield AE. Effect of regular budesonide and terbutaline on bronchial reactivity to allergen challenge. Am Rev Respir Dis 1992; 145: A54. 23 Robertson DG, Kerigan AT, Hargreave FE, Chalmers R, Dolovich J. Late asthmatic responses induced by ragweed pollen allergen. J Allergy Clin Immunol 1974; 54: 244-54.
24 Dolovich J, Hargreave FE, Chalmers R, Shier KJ, Gauldie J, Bienenstock J. Late cutaneous allergic responses in isolated IgEdependent reactions. J Allergy Clin Immunol 1973; 52: 38-46. 25 Kirby JG, Robertson DG, Hargreave FE, Dolovich J. Asthmatic responses to inhalation of anti-human IgE. Clin Allergy 1986; 16: 191-94. 26 van Schayck CP, Graafsma SJ, Visch MB, Dompeling E, van Weel C, van Herwaarden CLA. Increased bronchial hyperresponsiveness after inhaling salbutamol during 1 year is not caused by subsensitization to salbutamol. J Allergy Clin Immunol 1990; 86: 793-800. 27 Flint KC, Leung KBP, Hudspith BN, Brostoff J, Pearce FL, Johnson NM. Bronchoalveolar mast cells in extrinsic asthma: a mechanism for the initiation of antigen specific bronchoconstriction. BMJ 1985; 291: 923-26.
Citalopram for post-stroke pathological crying
Summary Post-stroke pathological crying is a distressing condition in which episodes occur in response to minor stimuli without associated mood changes. There is preliminary evidence of disturbed serotoninergic neurotransmission in such cases. We investigated the effect of the selective serotonin reuptake inhibitor citalopram on uncontrolled crying in stroke patients in a double-blind placebo-controlled crossover study. 16 consecutive patients (median age 58·5 years, range 40-83) entered the 9-week study a median of 168 days (range 6-913) post stroke and were treated with citalopram 10-20 mg daily for 3 weeks. Crying history was determined from semistructured interviews and from diaries kept by the patients. Psychiatric assessment was made with the Hamilton depression scale (HDS), and unwanted effects were measured with the UKU side-effect scale. In 13 patients in whom frequency of crying could be assessed, the number of daily crying episodes decreased by at least 50% in all cases during citalopram treatment vs 2 patients during placebo treatment (p<0 005, McNemar’s test), the effect being rapid (1-3 days) and pronounced in 11 (73%). There was a concomitant significant decrease in depression rating from HDS 8·9 to 5 3 (p<0 005, Wilcoxon’s test). Citalopram was well tolerated, the few side-effects being mild and transient. We conclude that serotoninergic neurotransmission plays an important part in post-stroke pathological crying and that citalopram is an effective and well-tolerated treatment.
Lancet 1993; 342: 837-39 See Commentary page 816
Introduction
pathological crying and/or laughing is a and distressing embarrassing complaint for the patient, is often socially disabling, and may interfere with rehabilitation. Patients with this condition have voluntary facial paroxysms that follow a fixed sequential pattern. Outbursts are triggered by minor non-specific stimuli, without any concomitant or subsequent change in mood.1 In some stroke patients episodes of profuse crying occur in
Post-stroke
Department of Neurology, Aalborg Hospital, 9000 Aalborg, Denmark (G Andersen MD, K Vestergaard MD, J O Riis PhD) Correspondence to: Dr Grethe Andersen
appropriate circumstances and it is unclear whether they have the same or a different disorder.2,3 The term emotionalism has been proposed to define the condition in which there is increased tearfulness with episodes of crying or laughing that are sudden or unheralded and not under normal social control. In one study the frequency of emotionalism was 11 % a year after stroke.2 Of the pharmacological approaches that have been studied for treatment of pathological crying,4-11 amitriptyline is said to be effective at a mean dose of 57-8 mg dayY During a study on post-stroke depression, we observed that, in patients in whom depression was treated openly with the selective serotonin reuptake inhibitor citalopram, there was a striking and immediate decrease in outbursts of crying. The same response has been noted with a similar drug, fluoxetin.8,9 Since no placebo-controlled clinical trial with these agents had been conducted, we undertook such a study of the effect of citalopram on uncontrolled crying in stroke patients.
per
Patients and methods 16 consecutive stroke patients with involuntary outbursts of crying referred over 7 months by general practitioners or by physicians in the Departments of Internal Medicine and
were
Neurology at Aalborg Hospital (a regional hospital serving a population of about 200 000). The study was approved by the local ethical committee and all patients or spouses gave signed consent. None of the patients had received post-stroke antidepressant treatment except for a short period immediately after the event in 1 case. Aphasic patients were included if a spouse could keep a diary. After a complete neurological examination, we evaluated cognitive function by use of a modified Danish version of the Mattis dementia rating scale.12 We used the Frenchay activities index13 to assess social function, and the Hamilton depression scale (HDS)14,15 for psychiatric assessment. Other tests included a semistructured interview modified from Lawson and Macleod4 to evaluate crying history; qualitative clinical evaluation of facial grimacing and concomitant crying equivalents (respiratory, secretory, or vasomotor changes); and assessment of the frequency of crying episodes with a five-point scale (none to continuous) and of the context in which episodes occurred with a three-point scale
(non-specific to emotionally provoked). In addition, patients kept a diary in which they recorded quantitative and qualitative (mild/ severe) data concerning crying. The study was conducted according to a double-blind placebocontrolled crossover protocol as follows: 7 days’ initial baseline registration, 21 days’ citalopram or placebo (randomised), 7 days’ washout, 7 days’ baseline registration, and crossover to second 21-day treatment period. Citalopram dose was 20 mg/day before 837
Figure
1:
Study design and analysis
bedtime for patients aged under 66 years and 10 mg/day for older patients. We measured unwanted effects with the UKU sideeffects rating scale,16 and evaluated patients on days 0, 7, 14, 28, 42, 49, and 63, as shown in figure 1. Medication containers were examined at the end of the study for assessment of compliance. We ascertained improvement in crying history from the clinical observations and interviews as well as from the patients’ diaries, and judged a reduction in recorded crying frequency of 50% or more to be significant. For patients with continuous crying, we assigned a score of 10 episodes/day.
Statistics Difference in response frequency (response being defined as > 50% reduction in the number of crying episodes) was analysed with McNemar’s test. Differences in crying frequency, HDS total score, and frequency/severity of side-effects were analysed with Wilcoxon matched-pairs signed-rank test. The non-parametric Friedman test was used to analyse the time factor and the interaction between treatment and time.
Results Clinical features
are shown in table 1. Median age of the 58-5 years and they entered the study patients consecutively a median of 168 days (range 6-913) post stroke. 6 patients fulfilled the classic criteria for was
pathological crying (ie, crying followed a fixed sequential pattern which they could not control and which was triggered by non-specific stimuli). Crying episodes in the other 10 patients were related to individual sensitive situations or subjects of conversation of an emotional nature. 1 of the patients with classic pathological crying (no 8) was withdrawn from study during the initial treatment period (placebo) because of a generalised seizure on day 28; 2 others (no 3 and no 9) did not complete the second treatment period (both placebo) because of lack of response after the first week. In the latter cases the self-registered score in the first week was therefore used as
to treatment
the
endpoint score. In another patient the first treatment period (citalopram) was slightly extended as the result of a misunderstanding. Finally,1 patient had a temporary pause after the first treatment period (citalopram) because crying episodes did not recur immediately. Apart from the fact that 1 patient was unable to keep a diary reliably, data from all 15 patients were included in the analysis. There were no demographic differences between patients treated with citalopram as the first or the second treatment. After 3 weeks of citalopram, 8 patients were free of crying episodes,1 cried mainly in emotional situations, and 6 cried exclusively when provoked emotionally. Of the 7 who still cried occasionally, 4 rated their crying episodes as being milder and shorter. Reduction in crying frequency as assessed by the interviewer (table 2) was significant at 2 and 4 weeks of citalopram (p < 0-001). Episodes of facial distress or grimacing without weeping provoked by non-specific stimuli were also analysed. After citalopram treatment, their frequency was reduced significantly (p<0-05) and they occurred exclusively in connection with emotionally provocative events. In 1 patient who initially had crying episodes there was a change to less frequent episodes of facial distress without weeping. The number of self-registered daily crying episodes is shown in figure 2, calculated as the mean for each week. By comparison with baseline, the reduction in mean daily episodes with citalopram from 4-46 to 1-11 per day was significant (p<0-05). Crying frequency was reduced by 50% or more in all patients treated with citalopram but in only 2 patients treated with placebo p < 0-005 (table 3). Reductions in crying determined by clinical assessment and patients themselves were in full agreement. Response to citalopram occurred immediately (within 24 h) in 8 patients, within 3 days in 3 patients, and more slowly in the remaining 4 patients (the 2 oldest patients and
*Fulfilled the classic criteria for pathological crying. †Lesions determined by computed tomography or magnetic resonance imaging. t0ut=outpat!ent; hosp = hospital inpatient. Table 1: Clinical features of 16 patients with post-stroke Involuntary crying
838
being able to tolerate higher doses. Our study shows that post-stroke pathological crying and emotionalism are basically the same condition, it being of little importance whether or not the crying episodes are non-specific or emotionally provoked. The most important
not
involuntary paroxysms of facial distress or grimacing. Although little is known about the natural course of pathological crying, there seems to be an association with symptoms of a more general post-stroke mood disturbance.2 One explanation is that depressive
feature is
Figure 2: Mean number of crying episodes per day Solid columns indicate initial citalopram followed columns placebo followed by citalopram.
by placebo and open
the 2 treated earliest post
stroke). All patients relapsed to crying episodes after stopping citalopram, although in most cases the frequency was less. 2 patients who forgot to take citalopram on one day had crying episodes the next day. No patient had major depression at the start of the study (total HDS > 17), but mean total HDS decreased from 89 to 5-3 after 3 weeks of citalopram (p < 0-005). did not detect any side-effects related to found a trend (p=0-06) in the global assessment of side-effects carried out by the investigatoreg, transient orthostatic dizziness, insomnia, or increased spasticity. Dose was temporarily reduced in 3 patients while on citalopram and in 1 while on placebo.
Although we citalopram we
Discussion Our results show that citalopram is very effective in the treatment of post-stroke pathological crying and emotionalism. Although we treated patients of widely different ages, with different vascular lesions, and at different times post stroke, the overall effect was favourable in all cases and we did not encounter any serious sideeffects. Response to citalopram was nearly always immediate, so is probably attributable to direct stimulation of serotoninergic neutrotransmission. Further evidence for a role of such neurotransmission is that amitriptyline, which is likewise effective, is also a potent serotonin reuptake inhibitor. The drawback with amitriptyline is that it is effective in only 75 % of cases at the doses used, patients
mood symptoms arise as a result of social isolation and fear of crying in public. Alternatively, both mood disturbance and pathological crying may have a common anatomical abnormality (eg, destruction of serotoninergic neurons or pathways), with serotoninergic neurotransmission consequently being reduced in both. In our patients citalopram treatment of pathological
crying led to a concomitant overall improvement depressive mood. However, we have insufficient data
in to
determine whether the effect on mood was as immediate as the effect on crying-ie, whether they have a common pathophysiology. In the amitriptyline study,!1 there was no indication of a pathophysiological link in that the doses used were lower than those usually recommended for antidepressive treatment, and no change in depression rating scores was detected. H Lundbeck A/ and Lundbeck Pharma A/S, Copenhagen, provided the citalopram and placebo tablets. Lundbeck Pharma A/also paid the patients’ transportation expenses and for secretarial assistance and statistical advice. We thank Mr Ove Aaskoven for the statistical analysis.
References Poeck K. Pathological laughter and crying. In: Fredericks JAM, ed. Handbook of clinical neurology, vol 1: clinical neuropsychology. Amsterdam: Elsevier, 1985: 219-25. 2 House A, Dennis M, Molyneux A, Warlow C, Hawton K. Emotionalism after stroke. BMJ 1989; 298: 991-94. 3 Allman P, Hope RA, Fairburn CG. Emotionalism following brain damage: a complex phenomenon. Postgrad Med J 1990; 66: 818-21. 4 Lawson JR, Macleod RDM. The use of imipramine ("Tofranil") and other psychotropic drugs in organic emotionalism. Br J Psychiatry 1969; 115: 281-85. 5 Wolf JK, Santana HB, Thorpy M. Treatment of "emotional incontinence" with levodopa. Neurology 1979; 29: 1435-36. 6 Schiffer RB, Cash J, Herndon RM. Treatment of emotional lability with low-dosage tricyclic antidepressants. Psychosomatics 1983; 24: 1094-96. 7 Udaka F, Yamao S, Nagata H, Nakamura S, Kameyama M. Pathologic laughing and crying treated with levodopa. Arch Neurol 1984; 41: 1
1095-96. 8
9 10
Non-parametric two-way analysis of variance: treatment, p < 0 001 (Wilcoxon test), time, p<0 001 (Friedman test); interaction treatment/time, p<0 001 (Fnedman test). Table 2: Crying frequency assessed by interviewer
McNemar’s test: X’= 09, df= 1, p=0 0026. *1 patient excluded (no self-registrations in second baseline period) and 1 patient unable to
keep diary reliably. Table 3: Comparison of treatment response
Seliger GM, Hornstein A, Flax J, Herbert J, Schroeder K. Fluoxetin improves emotional incontinence. Brain Inj 1992; 6: 267-70. Sloan RL, Brown KW, Pentland B. Fluoxetin as a treatment for emotional lability after brain injury. Brain Inj 1992; 6: 315-19. Ross ED, Stewart RS. Pathological display of affect in patients with depression and right frontal brain damage. J Nerv Ment Dis 1987; 175:
165-72. 11 Schiffer
RB, Herndon RM, Rudick RA. Treatment of pathologic laughing and weeping with amitriptyline. N Engl J Med 1985; 312:
1480-82. 12 Mattis S. Mental status examination for organic mental syndrome in the elderly patient. In: Bellak L, Karasu TB, eds. Geriatric psychiatry: a handbook for psychiatrists and primary care physicians. New York: Grune & Stratton; 1976: 77-121. 13 Holbrook M, Skilbeck CE. An activities index for use with stroke patients. Age Ageing 1983; 12: 166-70. 14 Hamilton M. A rating scale for depression. J Neurol Neurosurg Psychiatry 1960; 23: 56-62. 15 Beck P, Kastrup M, Rafaelsen OJ. Mini-compendium of rating scales for states of anxiety, depression, mania, schizophrenia with corresponding DSM-III syndromes. Acta Psychiatr Scand 1986; 74 (suppl 326): 7-37. 16 Lingjaerde O, Ahlfors UG, Bech P, Denker SJ, Elgren K. The UKU side effect rating scale. Acta Psychiatr Scand 1987; 76 (suppl 334): 1-99.
839
24 Dolovich J, Hargreave FE, Chalmers R, Shier KJ, Gauldie J, Bienenstock J. Late cutaneous allergic responses in isolated IgEdependent reactions. J Allergy Clin Immunol 1973; 52: 38-46. 25 Kirby JG, Robertson DG, Hargreave FE, Dolovich J. Asthmatic responses to inhalation of anti-human IgE. Clin Allergy 1986; 16: 191-94. 26 van Schayck CP, Graafsma SJ, Visch MB, Dompeling E, van Weel C, van Herwaarden CLA. Increased bronchial hyperresponsiveness after inhaling salbutamol during 1 year is not caused by subsensitization to salbutamol. J Allergy Clin Immunol 1990; 86: 793-800. 27 Flint KC, Leung KBP, Hudspith BN, Brostoff J, Pearce FL, Johnson NM. Bronchoalveolar mast cells in extrinsic asthma: a mechanism for the initiation of antigen specific bronchoconstriction. BMJ 1985; 291: 923-26.
Citalopram for post-stroke pathological crying
Summary Post-stroke pathological crying is a distressing condition in which episodes occur in response to minor stimuli without associated mood changes. There is preliminary evidence of disturbed serotoninergic neurotransmission in such cases. We investigated the effect of the selective serotonin reuptake inhibitor citalopram on uncontrolled crying in stroke patients in a double-blind placebo-controlled crossover study. 16 consecutive patients (median age 58·5 years, range 40-83) entered the 9-week study a median of 168 days (range 6-913) post stroke and were treated with citalopram 10-20 mg daily for 3 weeks. Crying history was determined from semistructured interviews and from diaries kept by the patients. Psychiatric assessment was made with the Hamilton depression scale (HDS), and unwanted effects were measured with the UKU side-effect scale. In 13 patients in whom frequency of crying could be assessed, the number of daily crying episodes decreased by at least 50% in all cases during citalopram treatment vs 2 patients during placebo treatment (p<0 005, McNemar’s test), the effect being rapid (1-3 days) and pronounced in 11 (73%). There was a concomitant significant decrease in depression rating from HDS 8·9 to 5 3 (p<0 005, Wilcoxon’s test). Citalopram was well tolerated, the few side-effects being mild and transient. We conclude that serotoninergic neurotransmission plays an important part in post-stroke pathological crying and that citalopram is an effective and well-tolerated treatment.
Lancet 1993; 342: 837-39 See Commentary page 816
Introduction
pathological crying and/or laughing is a and distressing embarrassing complaint for the patient, is often socially disabling, and may interfere with rehabilitation. Patients with this condition have voluntary facial paroxysms that follow a fixed sequential pattern. Outbursts are triggered by minor non-specific stimuli, without any concomitant or subsequent change in mood.1 In some stroke patients episodes of profuse crying occur in
Post-stroke
Department of Neurology, Aalborg Hospital, 9000 Aalborg, Denmark (G Andersen MD, K Vestergaard MD, J O Riis PhD) Correspondence to: Dr Grethe Andersen
appropriate circumstances and it is unclear whether they have the same or a different disorder.2,3 The term emotionalism has been proposed to define the condition in which there is increased tearfulness with episodes of crying or laughing that are sudden or unheralded and not under normal social control. In one study the frequency of emotionalism was 11 % a year after stroke.2 Of the pharmacological approaches that have been studied for treatment of pathological crying,4-11 amitriptyline is said to be effective at a mean dose of 57-8 mg dayY During a study on post-stroke depression, we observed that, in patients in whom depression was treated openly with the selective serotonin reuptake inhibitor citalopram, there was a striking and immediate decrease in outbursts of crying. The same response has been noted with a similar drug, fluoxetin.8,9 Since no placebo-controlled clinical trial with these agents had been conducted, we undertook such a study of the effect of citalopram on uncontrolled crying in stroke patients.
per
Patients and methods 16 consecutive stroke patients with involuntary outbursts of crying referred over 7 months by general practitioners or by physicians in the Departments of Internal Medicine and
were
Neurology at Aalborg Hospital (a regional hospital serving a population of about 200 000). The study was approved by the local ethical committee and all patients or spouses gave signed consent. None of the patients had received post-stroke antidepressant treatment except for a short period immediately after the event in 1 case. Aphasic patients were included if a spouse could keep a diary. After a complete neurological examination, we evaluated cognitive function by use of a modified Danish version of the Mattis dementia rating scale.12 We used the Frenchay activities index13 to assess social function, and the Hamilton depression scale (HDS)14,15 for psychiatric assessment. Other tests included a semistructured interview modified from Lawson and Macleod4 to evaluate crying history; qualitative clinical evaluation of facial grimacing and concomitant crying equivalents (respiratory, secretory, or vasomotor changes); and assessment of the frequency of crying episodes with a five-point scale (none to continuous) and of the context in which episodes occurred with a three-point scale
(non-specific to emotionally provoked). In addition, patients kept a diary in which they recorded quantitative and qualitative (mild/ severe) data concerning crying. The study was conducted according to a double-blind placebocontrolled crossover protocol as follows: 7 days’ initial baseline registration, 21 days’ citalopram or placebo (randomised), 7 days’ washout, 7 days’ baseline registration, and crossover to second 21-day treatment period. Citalopram dose was 20 mg/day before 837
Figure
1:
Study design and analysis
bedtime for patients aged under 66 years and 10 mg/day for older patients. We measured unwanted effects with the UKU sideeffects rating scale,16 and evaluated patients on days 0, 7, 14, 28, 42, 49, and 63, as shown in figure 1. Medication containers were examined at the end of the study for assessment of compliance. We ascertained improvement in crying history from the clinical observations and interviews as well as from the patients’ diaries, and judged a reduction in recorded crying frequency of 50% or more to be significant. For patients with continuous crying, we assigned a score of 10 episodes/day.
Statistics Difference in response frequency (response being defined as > 50% reduction in the number of crying episodes) was analysed with McNemar’s test. Differences in crying frequency, HDS total score, and frequency/severity of side-effects were analysed with Wilcoxon matched-pairs signed-rank test. The non-parametric Friedman test was used to analyse the time factor and the interaction between treatment and time.
Results Clinical features
are shown in table 1. Median age of the 58-5 years and they entered the study patients consecutively a median of 168 days (range 6-913) post stroke. 6 patients fulfilled the classic criteria for was
pathological crying (ie, crying followed a fixed sequential pattern which they could not control and which was triggered by non-specific stimuli). Crying episodes in the other 10 patients were related to individual sensitive situations or subjects of conversation of an emotional nature. 1 of the patients with classic pathological crying (no 8) was withdrawn from study during the initial treatment period (placebo) because of a generalised seizure on day 28; 2 others (no 3 and no 9) did not complete the second treatment period (both placebo) because of lack of response after the first week. In the latter cases the self-registered score in the first week was therefore used as
to treatment
the
endpoint score. In another patient the first treatment period (citalopram) was slightly extended as the result of a misunderstanding. Finally,1 patient had a temporary pause after the first treatment period (citalopram) because crying episodes did not recur immediately. Apart from the fact that 1 patient was unable to keep a diary reliably, data from all 15 patients were included in the analysis. There were no demographic differences between patients treated with citalopram as the first or the second treatment. After 3 weeks of citalopram, 8 patients were free of crying episodes,1 cried mainly in emotional situations, and 6 cried exclusively when provoked emotionally. Of the 7 who still cried occasionally, 4 rated their crying episodes as being milder and shorter. Reduction in crying frequency as assessed by the interviewer (table 2) was significant at 2 and 4 weeks of citalopram (p < 0-001). Episodes of facial distress or grimacing without weeping provoked by non-specific stimuli were also analysed. After citalopram treatment, their frequency was reduced significantly (p<0-05) and they occurred exclusively in connection with emotionally provocative events. In 1 patient who initially had crying episodes there was a change to less frequent episodes of facial distress without weeping. The number of self-registered daily crying episodes is shown in figure 2, calculated as the mean for each week. By comparison with baseline, the reduction in mean daily episodes with citalopram from 4-46 to 1-11 per day was significant (p<0-05). Crying frequency was reduced by 50% or more in all patients treated with citalopram but in only 2 patients treated with placebo p < 0-005 (table 3). Reductions in crying determined by clinical assessment and patients themselves were in full agreement. Response to citalopram occurred immediately (within 24 h) in 8 patients, within 3 days in 3 patients, and more slowly in the remaining 4 patients (the 2 oldest patients and
*Fulfilled the classic criteria for pathological crying. †Lesions determined by computed tomography or magnetic resonance imaging. t0ut=outpat!ent; hosp = hospital inpatient. Table 1: Clinical features of 16 patients with post-stroke Involuntary crying
838
being able to tolerate higher doses. Our study shows that post-stroke pathological crying and emotionalism are basically the same condition, it being of little importance whether or not the crying episodes are non-specific or emotionally provoked. The most important
not
involuntary paroxysms of facial distress or grimacing. Although little is known about the natural course of pathological crying, there seems to be an association with symptoms of a more general post-stroke mood disturbance.2 One explanation is that depressive
feature is
Figure 2: Mean number of crying episodes per day Solid columns indicate initial citalopram followed columns placebo followed by citalopram.
by placebo and open
the 2 treated earliest post
stroke). All patients relapsed to crying episodes after stopping citalopram, although in most cases the frequency was less. 2 patients who forgot to take citalopram on one day had crying episodes the next day. No patient had major depression at the start of the study (total HDS > 17), but mean total HDS decreased from 89 to 5-3 after 3 weeks of citalopram (p < 0-005). did not detect any side-effects related to found a trend (p=0-06) in the global assessment of side-effects carried out by the investigatoreg, transient orthostatic dizziness, insomnia, or increased spasticity. Dose was temporarily reduced in 3 patients while on citalopram and in 1 while on placebo.
Although we citalopram we
Discussion Our results show that citalopram is very effective in the treatment of post-stroke pathological crying and emotionalism. Although we treated patients of widely different ages, with different vascular lesions, and at different times post stroke, the overall effect was favourable in all cases and we did not encounter any serious sideeffects. Response to citalopram was nearly always immediate, so is probably attributable to direct stimulation of serotoninergic neutrotransmission. Further evidence for a role of such neurotransmission is that amitriptyline, which is likewise effective, is also a potent serotonin reuptake inhibitor. The drawback with amitriptyline is that it is effective in only 75 % of cases at the doses used, patients
mood symptoms arise as a result of social isolation and fear of crying in public. Alternatively, both mood disturbance and pathological crying may have a common anatomical abnormality (eg, destruction of serotoninergic neurons or pathways), with serotoninergic neurotransmission consequently being reduced in both. In our patients citalopram treatment of pathological
crying led to a concomitant overall improvement depressive mood. However, we have insufficient data
in to
determine whether the effect on mood was as immediate as the effect on crying-ie, whether they have a common pathophysiology. In the amitriptyline study,!1 there was no indication of a pathophysiological link in that the doses used were lower than those usually recommended for antidepressive treatment, and no change in depression rating scores was detected. H Lundbeck A/ and Lundbeck Pharma A/S, Copenhagen, provided the citalopram and placebo tablets. Lundbeck Pharma A/also paid the patients’ transportation expenses and for secretarial assistance and statistical advice. We thank Mr Ove Aaskoven for the statistical analysis.
References Poeck K. Pathological laughter and crying. In: Fredericks JAM, ed. Handbook of clinical neurology, vol 1: clinical neuropsychology. Amsterdam: Elsevier, 1985: 219-25. 2 House A, Dennis M, Molyneux A, Warlow C, Hawton K. Emotionalism after stroke. BMJ 1989; 298: 991-94. 3 Allman P, Hope RA, Fairburn CG. Emotionalism following brain damage: a complex phenomenon. Postgrad Med J 1990; 66: 818-21. 4 Lawson JR, Macleod RDM. The use of imipramine ("Tofranil") and other psychotropic drugs in organic emotionalism. Br J Psychiatry 1969; 115: 281-85. 5 Wolf JK, Santana HB, Thorpy M. Treatment of "emotional incontinence" with levodopa. Neurology 1979; 29: 1435-36. 6 Schiffer RB, Cash J, Herndon RM. Treatment of emotional lability with low-dosage tricyclic antidepressants. Psychosomatics 1983; 24: 1094-96. 7 Udaka F, Yamao S, Nagata H, Nakamura S, Kameyama M. Pathologic laughing and crying treated with levodopa. Arch Neurol 1984; 41: 1
1095-96. 8
9 10
Non-parametric two-way analysis of variance: treatment, p < 0 001 (Wilcoxon test), time, p<0 001 (Friedman test); interaction treatment/time, p<0 001 (Fnedman test). Table 2: Crying frequency assessed by interviewer
McNemar’s test: X’= 09, df= 1, p=0 0026. *1 patient excluded (no self-registrations in second baseline period) and 1 patient unable to
keep diary reliably. Table 3: Comparison of treatment response
Seliger GM, Hornstein A, Flax J, Herbert J, Schroeder K. Fluoxetin improves emotional incontinence. Brain Inj 1992; 6: 267-70. Sloan RL, Brown KW, Pentland B. Fluoxetin as a treatment for emotional lability after brain injury. Brain Inj 1992; 6: 315-19. Ross ED, Stewart RS. Pathological display of affect in patients with depression and right frontal brain damage. J Nerv Ment Dis 1987; 175:
165-72. 11 Schiffer
RB, Herndon RM, Rudick RA. Treatment of pathologic laughing and weeping with amitriptyline. N Engl J Med 1985; 312:
1480-82. 12 Mattis S. Mental status examination for organic mental syndrome in the elderly patient. In: Bellak L, Karasu TB, eds. Geriatric psychiatry: a handbook for psychiatrists and primary care physicians. New York: Grune & Stratton; 1976: 77-121. 13 Holbrook M, Skilbeck CE. An activities index for use with stroke patients. Age Ageing 1983; 12: 166-70. 14 Hamilton M. A rating scale for depression. J Neurol Neurosurg Psychiatry 1960; 23: 56-62. 15 Beck P, Kastrup M, Rafaelsen OJ. Mini-compendium of rating scales for states of anxiety, depression, mania, schizophrenia with corresponding DSM-III syndromes. Acta Psychiatr Scand 1986; 74 (suppl 326): 7-37. 16 Lingjaerde O, Ahlfors UG, Bech P, Denker SJ, Elgren K. The UKU side effect rating scale. Acta Psychiatr Scand 1987; 76 (suppl 334): 1-99.
839