(Stroke. 1997;28:1464-1466.)
© 1997 American Heart Association, Inc.
Articles |
Severe Pathological Crying After Left Anterior Choroidal Artery Infarct
Reversibility With Paroxetine Treatment
From the Service d'Urgences Neurovasculaires, Hôpital Neurologique, Lyon, France.
Correspondence to Dr L. Derex, Service d'Urgences Neurovasculaires, Hôpital Neurologique, 59 Boulevard Pinel, 69003 Lyon, France.
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Abstract |
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Background There is increasing evidence that serotonergic neurotransmission may be damaged in poststroke pathological crying. A correlation between the clinical severity of pathological crying and the size of stroke-induced serotonergic pathway lesions is commonly accepted. We present a case of severe pathological crying after a limited left anterior choroidal artery territory infarction.
Case Description A right-handed 55-year-old man who was a heavy smoker was admitted to the hospital after a right hemiplegia of sudden onset. Clinical examination revealed a right global hemiplegia including the face and a right hemihypoesthesia. Cerebral CT scan and MRI showed an infarct in the retrolenticular part of the posterior limb of the left internal capsule extending upward into the posterior paraventricular corona radiata region. Transesophageal echocardiography revealed an atrial septal aneurysm of 15-mm excursion without associated patent foramen ovale. From the first day of admission, the patient exhibited very frequent and intense fits of pathological crying. Their persistence led to initiation of treatment with the selective serotonin reuptake inhibitor paroxetine on day 30. Complete and immediate resolution of pathological crying occurred 24 hours after onset of therapy. Follow-up examination at day 90 confirmed the absence of relapse of pathological crying.
Conclusions We conclude that poststroke pathological crying in our patient may have been due to unilateral disruption of the capsular ascending projections of the serotonergic brain stem raphe nuclei. A small left-sided capsular lesion may have led to severe pathological crying. This disabling condition may be reversible with selective serotonin reuptake inhibitor therapy.
Key Words: crying • emotions • subcortical infarction • serotonin
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Introduction |
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The anterior choroidal artery (AChA) syndrome was described in 1925 by Foix et al.1 Its complete form includes a triad of hemiplegia, hemisensory loss, and hemianopia, but incomplete forms are more frequent. Patients with AChA territory infarct may display abnormalities of higher function, but data concerning emotional regulation impairment after unilateral AChA territory infarct are scarce. We report a case of prolonged pathological crying (PC) after left AChA territory infarct. This poststroke PC was immediately and permanently reversed with selective serotonin reuptake inhibitor therapy.
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Case Report |
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TopAbstractIntroductionCase ReportDiscussionReferences |
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A right-handed 55-year-old man who was a heavy smoker was admitted to the hospital after a right hemiplegia of sudden onset on November 21, 1995. He had had a left lower limb thrombophlebitis at the age of 54 years.
At the time of hospital admission the patient was alert, and clinical examination revealed a right global hemiplegia including the face, a right Babinski's sign, and a right hemihypoesthesia. The patient could not feel pinprick, deep pain, touch, or vibratory stimuli in his right limbs. He was dysarthric, but language use, repetition, and comprehension were normal. No homonymous hemianopia and no visual neglect were noted. Blood pressure was 135/85 mm Hg.
Initial cerebral CT scan was normal. Control CT scan and brain MRI
showed an infarct in the retrolenticular part of the posterior limb of
the left internal capsule extending upward into the posterior
paraventricular corona radiata region
(Figure
). The left AChA did not fill on cerebral
angiography performed at day 8, which was otherwise normal. Visual
field was normal at day 8. Baseline and 24-hour
electrocardiograms were normal.
Transesophageal echocardiography
revealed an atrial septal aneurysm of 15-mm excursion without
associated patent foramen ovale, right-left shunt, mitral valve
prolapse, or left atrial spontaneous echo contrast. A mild aortic arch
atherosclerotic plaque was noted. Repeated extensive research for
prothrombotic states was negative.
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From the first day of admission, the patient exhibited very frequent fits of pathological crying (five to eight times a day), bursting into tears without apparent affective determination. These episodes were extremely intense, lasting from 1 to 2 minutes, uncontrollable by the patient. They were generally precipitated by trivial environmental stimuli and were mood incongruent. Although concerned with his hemiplegia, the patient showed no signs of depression and in particular never expressed emotional pain. The Hamilton Depression Rating Scale was in the normal range. These manifestations decreased in frequency during the first month, but the intensity of the outbursts did not diminish with time. Their persistence (three episodes per day) led to initiation of treatment on day 30 with the selective serotonin reuptake inhibitor paroxetine (Deroxat, Smithkline Beecham) 20 mg/d. Complete and immediate resolution of these episodes occurred 24 hours after onset of therapy. Follow-up examination at 12 months confirmed the absence of relapse of pathological crying. The patient remained hemiparetic and was able to walk with assistance for 100 m.
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Discussion |
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Uncontrollable fits of laughter or crying, generally devoid of emotional content and precipitated by minor affective or neutral events, may be observed in patients with lesions in diverse areas in the cortex, diencephalon, and brain stem, but in most instances, lesions involving systems affecting motor function (pyramidal tract or extrapyramidal fiber lesions) and an interruption of a control system supposedly located at the base of the brain stem are observed.2 This disruption of proper emotional expression may be stroke induced and has variously been labeled emotional incontinence, emotional dysregulation, or emotionalism.3
Specific data related to emotional expression in patients with AChA territory infarcts are scarce. Cambier et al4 focused on neuropsychological impairment in patients with AChA territory infarcts depending on the site of infarction. Right-sided lesions may lead to visual neglect, constructional apraxia, anosognosia, and motor impersistence. Slight disorders of speech may be present in left-sided lesions, resembling the symptoms of thalamic aphasia, with impaired fluency, difficulty in organizing speech, and rare semantic paraphasias but sparing of repetition and comprehension.5 Impairment of emotional regulation has rarely been reported in patients with unilateral AChA territory infarct. Helgason et al6 reported eight cases of acute pseudobulbar mutism due to bilateral capsular infarction in the territory of the AChA. The majority had a period of lethargy. Four patients had uncontrollable fits of laughter or crying devoid of emotional content, and others had depression or blunted affect. The case of our patient, in whom a single ischemic capsular lesion was observed, illustrates the emotional aspect of unilateral left AChA territory infarcts.
Many authors have compared the mood of patients with unilaterally right- and left-sided brain damage and discussed the possible lateralization of emotional expression. Whereas some studies have suggested that frequency and severity of depression were greater with left than with right hemisphere lesions7 or that the severity of depression was significantly increased in patients with left anterior lesions,8 other prospective studies have shown a more complex relationship between size, location, and side of the lesion9 or have shown no evidence of a difference between right and left hemisphere stroke in the nature of the relationship between lesion distribution and mood symptoms.10 11
There is indirect evidence that serotonergic neurotransmission may be damaged in patients with poststroke PC. In our patient, response to paroxetine was immediate and thus probably attributable to direct stimulation of serotonergic neurotransmission. The same response of poststroke PC has been noted with other selective serotonin reuptake inhibitors, such as fluoxetine12 and citalopram.13 Amitriptyline, which is also a potent serotonin reuptake inhibitor, is likewise effective at a mean dose of 57.8 mg/d but was effective in only 75% of cases at the doses used, since patients were not able to tolerate higher doses.14 Poststroke PC may be attributable to stroke-induced partial destruction of the serotonergic raphe nuclei in the brain stem or their ascending projections to the hemispheres.15 The serotonergic raphe nuclei in the brain stem give rise to long projections to the limbic forebrain structures. The principal ascending fibers arise from serotonin cell bodies located in the dorsal nucleus of the raphe and in the superior central nucleus. The major ascending pathway from the rostral raphe nuclei joins the medial forebrain bundle in the lateral hypothalamus. Fibers leaving this main ascending bundle enter the substantia nigra, the intralaminar thalamic nuclei, the stria terminalis, the septum, and the internal capsule.16 Andersen et al15 have recently proposed a pathoanatomic correlation between the severity of poststroke PC and the extent of damage to brain areas involved in serotonergic neurotransmission. In their study the patients with severe poststroke PC had large bilateral pontine or central hemispheric lesions, and the clinically least affected patients had mainly unilateral large subcortical lesions. In contrast, in our patient brain MRI ruled out a lesion of the brain stem or of the temporal lobe regions supplied by the AChA, particularly the uncus, the posteromedial half of the amygdala, and the anterior hippocampus.17 The poststroke PC experienced by our patient was severe and long-lasting. The magnitude of spontaneous reduction of PC frequency during the first month after stroke was only approximately 40%. By day 30 the outbursts were very distressing, and their intensity did not diminish with time. We conclude that a single limited subcortical left-sided lesion with a critical topography regarding serotonergic pathways may cause permanent PC. This condition may be attributable to stroke-induced unilateral left damage of the capsular ascending projections of the serotonergic raphe nuclei.
Received February 10, 1997; revision received March 24, 1997; accepted April 25, 1997.
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References |
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