Seven patients demonstrated only episodes of PC, two patients demonstrated only episodes of PL, and the remaining patient demonstrated both episodes of crying and laughing. However, all patients developed PLC within 6 months after TBI. The prevalence of PLC was 3.3% at the initial evaluation, 7.1% at 3 months, 6.1% at 6 months, and 1.7% at 12 months. There were 10 (10.9%) out of 92 TBI patients who met our criteria for PLC. Background, neurological, and neuroradiological data were registered and recorded using Traumatic Coma Data Bank forms. In addition, the occurrence of medical complications such as hypoxia or arterial hypotension that might have contributed to secondary brain damage was assessed. The posttraumatic amnesia period was estimated retrospectively using a structured interview that has been shown to have a high correlation with prospective determinations of posttraumatic amnesia. 21 The second measure of severity of TBI was based on the length of posttraumatic amnesia. 20 Patients with a Glasgow Coma Scale score in the 12–15 range but who underwent intracranial surgical procedures or presented with focal lesions greater than 15 cc total volume were considered to have moderate head injury. According to this measure, Glasgow Coma Scale scores of 13–15 define mild head injury, 9–12 define moderate head injury, and 4–8 define severe head injury. The first measure was the 24-hour Glasgow Coma Scale score. We hypothesized that PLC was associated with damage to the prefrontal cortex and the presence of mood or anxiety disorders. In this study, the clinical correlates and the clinical course of PLC following TBI were examined. 2, 16, 17 Using double blind methodology, previous studies have demonstrated that PLC responds to amitriptyline, 17 nortriptyline, 2 citalopram, 16 and sertraline. 2 There is also considerable evidence that PLC responds to treatment with antidepressants. This scale has high reliability and demonstrated validity and has been used to effectively rate PLC in patients with different neurological disorders. 16 We have developed a quantitative scale to measure and quantify the severity of PLC, termed the Pathological Laughter and Crying Scale. 15īecause PLC can be socially disabling, it may interfere with a patient’s rehabilitation process. 9, 13, 14 On the other hand, there have been few studies that have examined the association between PLC and the presence of anxiety disorders. Some studies reported that PLC was associated with the presence of major depression, 1, 3, 12 while others reported no association. Previous studies focused on the relationship between PLC and major depression. The relationship between PLC, mood disorders, and anxiety disorders has not been consistently established. Patients with PLC had a greater severity of brain injury and other neurological features compatible with pseudobulbar palsy. 11 reported the occurrence of PLC in 16 out of 301 patients with severe TBI consecutively admitted to a rehabilitation unit. There have been few studies focusing on PLC following traumatic brain injury (TBI). 10 suggested that the critical lesions eliciting PLC are located along fronto-ponto-cerebellar pathways. 9 studied ALS patients with and without PLC and implicated the prefrontal cortex in the pathophysiology of pathological affect. Ross and Rush 8 hypothesized that pathological affect could be observed in patients with lesions of the right inferior frontal lobe in association with a major depressive disorder. However, PLC may also be seen in patients with unilateral lesions that do not involve motor or premotor areas. 7 Thus, PLC is an essential part of the pseudobulbar palsy syndrome that is the consequence of bilateral lesions in corticobulbar pathways. According to these assumptions, PLC results from the release of cortical inhibition of upper brainstem centers that integrate the motor activation patterns involved in laughing and crying. 5, 6Ĭlassic pathophysiological theories of PLC are based on the assumptions of serial processing and hierarchical control. It has been reported that the prevalence of PLC is approximately 10%–20% among patients with stroke, 1, 2 40% among patients with Alzheimer’s disease (AD), 3 7%–10% among patients with multiple sclerosis, 4 and 19%–49% among patients with amyotrophic lateral sclerosis (ALS). In addition, PLC is a relatively frequent consequence of brain damage. Pathological laughing and crying (PLC) can be described as uncontrollable episodes of laughing or crying that are triggered by a stimulus that would not normally cause such an emotional response.
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