Abstract
A 42-year-old man was referred to the psychiatric department on the eighth day after cranioplasty in November 2008 due to his involuntary and uncontrollable outbursts of laughter. About two months prior, he had experienced a sudden severe headache, was diagnosed with acute subdural and subarachnoid haemorrhages in the fronto-temporo-parietal area of his brain, and underwent an emergency surgical procedure in our hospital. Following subsequent surgery for cranioplasty two months later, he began experiencing unexpected and uncontrollable episodes of laughter regardless of his emotional state or external situation. These bouts of laughing occurred several times a day and lasted for a few minutes on each occasion. This condition was embarrassing for him and resulted in considerable impairment with respect to his social relationships. He had no prior history of any physical or psychiatric illnesses and his condition was diagnosed as pathologic laughing. He was prescribed paroxetine (12.5 mg/day) to treat the problem. On the third day of paroxetine administration, he experienced a feeling of rigidity in his tongue and oral muscles, and showed poor articulation of speech. Tests revealed no interval change of any neurologic sign or laboratory finding over this period. Subsequently, paroxetine was ceased and the dysarthria disappeared a few days later.
Pathological laughing denotes paroxysms of sudden and involuntary laughter, a condition which is often found in patients with brain lesions. Paroxetine has been reported to be an effective treatment for pathological laughing and crying caused by stroke and traumatic brain injury [1]. Our patient became dysarthric after three days of paroxetine treatment. There are many causes of dysarthria, one of which can be rigidity of oral muscles due to drug-induced extrapyramidal symptoms (EPS). In the present case, the dysarthria could be considered as paroxetine-induced because it first appeared soon after the start of the paroxetine treatment and stopped when the drug was discontinued.
Although selective serotonin reuptake inhibitor (SSRI)-induced EPS is a low frequency adverse event, it can be uncomfortable for patients and can contribute to significant psychosocial impairment. Serotonergic projections from the dorsal raphe to the substantia nigra are known, and this system appears to have inhibitory effects on the nigrostriatal dopaminergic tract [2]. It has been suggested that SSRI-induced EPS could result from increased serotonergic neurotransmission, which antagonizes dopaminergic neurotransmission in the nigrostriatal pathway. In humans, the substantia nigra has the highest concentration of paroxetine binding sites [3]. Furthermore, a history of central nervous system damage has been suggested as a potential risk factor for SSRI-induced EPS [4].
With his brain injury, our patient would have been at increased risk for SSRI-induced EPS and his vulnerability may have been increased through paroxetine administration. SSRIs have been widely prescribed in patients with brain lesions resulting, for example, from cerebral haemorrhage, brain tumours, and traumatic brain injury. Although the appearance of EPS has been a rare adverse reaction to SSRIs, this report supports the assertion that clinicians should be aware of the possibility of SSRI-induced EPS in susceptible patients, especially in those with brain lesions.