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During rehabilitation from a severe traumatic brain injury, a 16‐year‐old girl became aware that she had lost the ability to laugh out loud. This rare phenomenon previously has been described as “aphonogelia.” A discussion of therapeutic avenues that were explored with this patient is presented in the first case, to our knowledge, of aphonogelia after a traumatic brain injury.
Level of Evidence
Pseudobulbar affect (PBA) is defined by episodes of involuntary crying and/or laughing as a result of brain injury or other neurological disease. Epidemiology studies show that 5.3%-48.2% of people with traumatic brain injury (TBI) may have symptoms consistent with (or suggestive of) PBA. Yet it is a difficult and often overlooked condition in individuals with TBI, and is easily confused with depression or other mood disorders. As a result, it may be undertreated and persist for longer than it should. This review presents the signs and symptoms of PBA in patients with existing TBI and outlines how to distinguish PBA from other similar conditions. It also compares and contrasts the different diagnostic criteria found in the literature and briefly mentions appropriate treatments. This review follows a composite case with respect to the clinical course and treatment for PBA and presents typical challenges posed to a provider when diagnosing PBA.
Emotionalism is an heightened tendency to cry, or more rarely, laugh. It is commonly associated with brain damage and is often distressing to both patients and carers. Emotionalism is easily confused with depression, and when severe it can interfere with treatment. The aetiology is poorly understood but its response to drugs with different modes of action suggests that there is more than one underlying mechanism. When the components of emotionalism are studied separately a wide range is observed and they combine in a more complex and varied way than commonly held stereotyped views suggest. Most patients with emotionalism are helped by simple education and reassurance. Some severe cases respond dramatically to tricyclic antidepressants, levodopa or fluoxetine.
Available treatments for depression have significant limitations, including low response rates and substantial lag times for response. Reports of rapid antidepressant effects of a number of compounds, including the glutamate N-methyl-D-aspartate receptor antagonist ketamine, have spurred renewed translational neuroscience efforts aimed at elucidating the molecular and cellular mechanisms of action that result in rapid therapeutic response. This perspective provides an overview of recent advances utilizing compounds with rapid-acting antidepressant effects, discusses potential mechanism of action and provides a framework for future research directions aimed at developing safe, efficacious antidepressants that achieve satisfactory remission not only by working rapidly but also by providing a sustained response.Molecular Psychiatry advance online publication, 21 May 2013; doi:10.1038/mp.2013.55.
Although laughter and humour have been constituents of humanity for thousands if not millions of years, their systematic study has begun only recently. Investigations into their neurological correlates remain fragmentary and the following review is a first attempt to collate and evaluate these studies, most of which have been published over the last two decades. By employing the classical methods of neurology, brain regions associated with symptomatic (pathological) laughter have been determined and catalogued under other diagnostic signs and symptoms of such conditions as epilepsy, strokes and circumspect brain lesions. These observations have been complemented by newer studies using modern non-invasive imaging methods. To summarize the results of many studies, the expression of laughter seems to depend on two partially independent neuronal pathways. The first of these, an 'involuntary' or 'emotionally driven' system, involves the amygdala, thalamic/hypo- and subthalamic areas and the dorsal/tegmental brainstem. The second, 'voluntary' system originates in the premotor/frontal opercular areas and leads through the motor cortex and pyramidal tract to the ventral brainstem. These systems and the laughter response appear to be coordinated by a laughter-coordinating centre in the dorsal upper pons. Analyses of the cerebral correlates of humour have been impeded by a lack of consensus among psychologists on exactly what humour is, and of what essential components it consists. Within the past two decades, however, sufficient agreement has been reached that theory-based hypotheses could be formulated and tested with various non-invasive methods. For the perception of humour (and depending on the type of humour involved, its mode of transmission, etc.) the right frontal cortex, the medial ventral prefrontal cortex, the right and left posterior (middle and inferior) temporal regions and possibly the cerebellum seem to be involved to varying degrees. An attempt has been made to be as thorough as possible in documenting the foundations upon which these burgeoning areas of research have been based up to the present time.
The effects of brain damage on cognitive and affective status have been assessed separately; however, a dearth of information exists about the interaction of these facets in the brain-damaged patient. Because appreciation of humour involves both cognitive and affective dimensions, an investigation of response to humorous materials should yield information relevant to this issue. In addition, a study of response to humour in aphasic patients can reveal the extent to which appreciation of humour is dependent upon an intact language system. Accordingly a test of humour, in which an individual chose the "funniest" of four cartoons, was administered to a population of brain-damaged and control patients. Ability to detect the most humorous cartoon was impaired in all brain-damaged patients, more in severe than in mild aphasics, but there was no significant difference between patients with left and right hemisphere lesions in their overall performance on the test. A different order of difficulty across items, and a different profile of "mirth" responses to the items did, however, correlate with site of lesion. Right hemisphere patients tended either to laugh throughout or, more frequently, not at all; they often confabulated answers to made impossible inferences; and they performed better on items with captions. Their cognitive reactions appeared "dissociated" from their affective responses. In contrast left hemisphere patients performed better on the captionless items and behaved in a manner which more closely approximated normal subjects in their humorous reactions, their order of item difficulty, and their explanations. All brain-damaged patients found it relatively easier to locate the humorous cartoons when the members of a set differed appreciably from one another. These results provide information about the altered cognitive and affective states of brain-damaged patients, the impairment of cognitive operations in aphasic patients, and the respective "life-spaces" of left and right hemisphere injured patients.
Laughter is an affective nonspeech vocalization that is not reserved to humans, but can also be observed in other mammalians, in particular monkeys and great apes. This observation makes laughter an interesting subject for brain research as it allows us to learn more about parallels and differences of human and animal communication by studying the neural underpinnings of expressive and perceptive laughter. In the first part of this review we will briefly sketch the acoustic structure of a bout of laughter and relate this to the differential anatomy of the larynx and the vocal tract in human and monkey. The subsequent part of the article introduces the present knowledge on behavioral and brain mechanisms of “laughter-like responses” and other affective vocalizations in monkeys and apes, before we describe the scant evidence on the cerebral organization of laughter provided by neuroimaging studies.