Transcript 投影片 1
Psychiatric care of traumatic brain injury 謝光煬 台灣大學醫學士暨理學博士 奇美醫學中心精神科主治醫師 南台科技大學生科所助理教授 Epidemiology of traumatic brain injury (TBI) Leading causes: motor vehicle crashes, falls, struck by/against events, violence. High risk groups: adolescents and young adults, people older than 75 years of age. Male-to-female ratio = 2:1 Mortality rate: 5-6 % Prevalence of TBI-related long-term disability in general population: 1-2 % Pathology of TBI Penetrating or closed injury Epidural hemorrhage Subdural hemorrhage Subarachnoid hemorrhage Intracerebral hemorrhage Contusion Diffuse axonal injury Sequelae of TBI Individual and variable Neurological symptoms: Seizure Blurred or double vision (diplopia) Motor disorders: weakness in limbs or facial muscles, muscle spasm, incoordination of movements, unsteady gait. Sensory disorders: tingling, numbness, pain. Aphasia, slurred speech, dysphagia. Dizziness, headache, vertigo. Psychiatric symptoms Psychiatric symptoms of TBI Cognitive symptoms: decreased attention, decreased speed in information processing, impaired executive function, problems with memory and learning new information. Mood symptoms: depression, anxiety, irritability, impulsivity, disinhibition, emotional lability, inappropriate affect. Psychotic symptoms: delusion, hallucination, catatonia. Personality change, behavior problem (agitation, aggression, disturbing). Pathogenesis of posttraumatic psychiatric disturbance Preinjury factors: age, gender, neurogenetics, baseline cognitive function, psychiatric conditions, substance abuse, socioeconomic environment, and risk-taking behaviors. Injury characteristics: location, type, and severity of neural damage. Postinjury factors: social support, timely medical and rehabilitative treatments, socioeconomic status, and medicolegal issues. (Am J Psychiatry. 2009; 166:653–661) Natural course of TBI (1) Stages of recovery: Acute stage: to stabilize the patient immediately after the injury. Subacute stage: to rehabilitate and return the patient to the community. Chronic stage: to continue rehabilitation and treat the long-term impairments. Natural course of TBI (2) There is a period of posttraumatic amnesia or confusion, defined as occurring between the time of injury and the return of continuous memory. A 6- to 12-month period of spontaneous recovery follows. After this period, remaining symptoms are likely to be permanent. Long-term outcome: 22.2% improved, 15.2% declined, and 62.6% unchanged from 1 year after injury to 5 years. (J Head Trauma Rehabil. 2001; 16:343-55.) Indicators of prognosis Duration of coma: the shorter the coma, the better the prognosis. Posttraumatic amnesia/confusion: the shorter this period, the better the prognosis. Age: patients over 60 or under 2 years old have the worst prognosis. Pharmacological strategies for neuroprotection in TBI Strategies targeting inflammation, oxidative damage, glutamate excitotoxicity, cell death and regeneration have been proposed and under investigation. Psychiatric pharmacotherapy at acute/subacute stage of TBI Posttraumatic amnesia/confusion or delirium is the major psychiatric problem at acute/subacute stage of TBI. However, using antipsychotics at this period has a negative impact on cognitive recovery. It results in 7 more days required to clear posttraumatic amnesia. (Brain Inj. 2006; 20:905-11.) Avoid giving antipsychotics at this stage unless there is confusion or delirium with significant behavior problem. Use 2nd-generation antipsychotics since they have less negative effects on cognitive recovery. Psychiatric pharmacotherapy at subacute/chronic stages of TBI Psychiatric symptoms at subacute/chronic stage of TBI need appropriate intervention since they impede the recovery process and rehabilitation. Patients with moderate to severe TBI who developed mood disorders had significantly smaller hippocampal volumes and worse vocational outcomes at 1-year follow-up than patients with equivalent severe TBI who did not develop mood disturbance. (Biol Psychiatry. 2007; 62:332-8. ) Current practice is a symptom-based approach. Points for attention about psychiatric pharmacotherapy of TBI Be aware that patients with TBI are especially sensitive to extrapyramidal symptoms. Sedative and anticholinergic effects of medications may impede cognitive functions. Start low and go slow. Be careful of the motor and cognitive effects of medications. Assess risk and benefit. Treating cognitive symptoms Stimulants: methylphenidate 20-40 mg/d recommended for increasing attention and speeding up information processing. Also effective for depression. Cholinergic agents: donepezil 5-10 mg/d recommended for improving attention and memory. Dopaminergic agents: amantadine, bromocriptine. Treating behavioral symptoms Beta-blockers: propranolol 20-160 mg/d recommended for aggression or agitation. Underlying mood or psychotic symptoms should be treated. Treating mood symptoms Antidepressants: sertraline and other selective serotonin reuptake inhibitors (SSRIs) for depression and anxiety. Anticonvulsants: valproate for irritability, impulsivity and posttraumatic epilepsy. Be careful of sedative and muscle-relaxing effects of benzodiazepines. Avoid using them in patients with TBI. Treating psychotic symptoms It has been proposed that 2nd-generation antipsychotics should be the primary agents for psychosis and significant agitation after TBI. There are some case reports and case series using risperidone, ziprasidone, quetiapine, olanzapine, or clozapine in TBI, mostly for the management of agitation. There is a lack of literature about zotepine, aripiprazole and amisulpride in TBI. Neuropsychological and occupational assessment To evaluate the degree of damage and recovery To help application for disability certificate and welfare To provide evidence for lawsuit or litigation Holistic care of TBI Neuropsychiatric pharmacotherapy Neuropsychological rehabilitation Psychotherapy, cognitive behavioral therapy Social welfare and support Thanks for attention