Biomedical subjects

David B. Arciniegas

Publications and source records attributed to David B. Arciniegas.

4 recordsLinked to original sources

PubMed2002

Cognitive Impairment Following Traumatic Brain Injury.

Cognitive impairments due to traumatic brain injury (TBI) are substantial sources of morbidity for affected individuals, their family members, and society. Disturbances of attention, memory, and executive functioning are the most common neurocognitive consequences of TBI at all levels of severity. Disturbances of attention and memory are particularly problematic, as disruption of these relatively basic cognitive functions may cause or exacerbate additional disturbances in executive function, communication, and other relatively more complex cognitive functions. Because of the high rate of other physical, neurologic, and psychiatric syndromes following TBI, a thorough neuropsychiatric assessment of the patient is a prerequisite to the prescription of any treatment for impaired cognition. Psychostimulants and other dopaminergically active agents (eg, methylphenidate, dextroamphetamine, amantadine, levodopa/carbidopa, bromocriptine) may modestly improve arousal and speed of information processing, reduce distractibility, and improve some aspects of executive function. Cautious dosing (start-low and go-slow), frequent standardized assessment of effects and side effects, and monitoring for drug-drug interactions are recommended. Cognitive rehabilitation is useful for the treatment of memory impairments following TBI. Cognitive rehabilitation may also be useful for the treatment of impaired attention, interpersonal communication skills, and executive function following TBI. This form of treatment is most useful for patients with mild to moderate cognitive impairments, and may be particularly useful for those who are still relatively functionally independent and motivated to engage in and rehearse these strategies. Psychotherapy (eg, supportive, individual, cognitive-behavioral, group, and family) is an important component of treatment. For patients with medication- and rehabilitation-refractory cognitive impairments, psychotherapy may be needed to assist both patients and families with adjustment to permanent disability.

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PubMed2002

Post-traumatic Headache.

Headache is the most common symptom after closed head injury, persisting for more than 2 months in 60% of patients. Rarely does headache occur in isolation. Cervical pain is a frequent accompaniment. Post-traumatic headache is often one of several symptoms of the postconcussive syndrome, and therefore may be accompanied by additional cognitive, behavioral, and somatic problems. Acute post-traumatic headaches may begin at the time of injury and continue for up to 2 months post-injury. Although onset proximate to the time of injury is most common, any new headache type occurring within this period of time is referred to as an acute post-traumatic headache. If such headaches persist beyond the first two months post-injury, they are subsequently referred to as chronic post-traumatic headaches. Over time, post-traumatic headaches may take on a pattern of daily occurrence. If aggressive treatment is initiated early, posttraumatic headache is less likely to become a permanent problem. Once "windup" of post-traumatic headaches occurs, the cycle of ongoing headaches is more difficult to interrupt. The mechanism of post-traumatic headache is poorly understood. Trauma-induced headaches are usually heterogeneous in nature, often including both tension-type pain and intermittent migraine-like attacks. Rebound-headaches may develop from overuse of analgesic medications, and the occurrence of such may complicate significantly the diagnosis of post-traumatic headache. Adequate treatment typically requires both "peripheral" and "central" measures. Understanding the general principles of treatment, especially appropriate use of preventive and abortive medications, will most usefully guide treatment. There is scant literature with which to direct treatment selection for post-traumatic headache. Consequently, treatments for post-traumatic headache are based on those prescribed for phenomenologically similar but etiologically distinct headache disorders. Delayed recovery from post-traumatic headache may be a result of inadequately aggressive or ineffective treatment, overuse of analgesic medications resulting in analgesia rebound phenomena, or comorbid psychiatric disorders (eg, post-traumatic stress disorder, insomnia, substance abuse, depression, or anxiety).

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PubMed2002

Suicide in Neurologic Illness.

The risk of attempted or completed suicide is increased in patients with migraine with aura, epilepsy, stroke, multiple sclerosis, traumatic brain injury, and Huntington's disease. Contrary to the general perception that the risk of suicide among patients with Alzheimer's disease and other dementing conditions is low, several reports suggest that the risk of suicide in these patients increases relative to the general population. Some patients at risk for neurologic disorders are also at increased risk for suicide; in particular, the risk of suicide is increased among persons at risk for Huntington's disease, independent of the presence or absence of the Huntington's gene mutation. The risk of attempted or completed suicide in neurologic illness is strongly associated with depression, feelings of hopelessness or helplessness, and social isolation. Additional suicide risk factors in persons with neurologic illness include cognitive impairment, relatively younger age (under 60 years), moderate physical disability, recent onset or change in illness, a lack of future plans or perceived meaning in life, recent losses (personal, occupational, or financial), and prior history of psychiatric illness or suicidal behavior. Substance dependence, psychotic disorders, anxiety disorders, and some personality disorders (eg, borderline personality disorder) may also contribute to increased risk of suicide among persons with neurologic illnesses. Identification and aggressive treatment of psychiatric problems, especially depression, as well as reduction of modifiable suicide risk factors among patients with neurologic illness is needed to reduce the risk of attempted and completed suicide in this population.

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PubMed2001

Psychosis Due to Neurologic Conditions.

Psychosis arises with considerable frequency in a number of neurologic conditions. The treatment of such patients is often challenging, as many of the treatments for psychosis pose some risk of worsening the underlying neurologic condition. Although psychosis may emerge in the context of any neurologic condition that sufficiently disrupts the functioning of or connections between limbic, paralimbic, frontal, subcortical areas mediating complex sensory perception, interpretation, and thought or language organization, secondary psychoses are most often encountered in patients with Alzheimer's disease (Parkinson's disease receives dopaminomimetic therapies) and epilepsy. Psychosis, and particularly delusions and visual hallucinations, may arise in Alzheimer's disease. Based on the available literature, the first-line therapy for this problem is risperidone 0.5 to 3 mg per day. If this treatment proves unsuccessful, low-dose haloperidol or olanzapine should be considered next. If these treatments prove unsuccessful, quetiapine should then be considered. Finally, clozapine may be useful for treatment-refractory psychosis due to Alzheimer's disease, but due caution is warranted given its considerable anticholinergic properties and potential for worsening cognition in these patients. Although disease-emergent psychosis (paranoid delusions and visual hallucinations) may develop in patients with Parkinson's disease, psychosis due to dopaminomimetic therapy is much more common. When such symptoms develop, the accepted first step is to taper anti-parkinsonian medications were possible. Anticholinergic medications, amantadine, selegiline, and dopamine receptor agonists should be reduced or discontinued, provided that the patient can tolerate changes in motor symptoms attendant to such reductions. When these reductions are not feasible or fail to improve treatment-emergent psychosis, low-dose quetiapine or clozapine may be useful. The greatest body of evidence supports the effectiveness of these treatments and their relative lack of adverse effects on motor function. When psychosis develops in the context of epilepsy, the generally accepted first step is to maximize anticonvulsant therapy in an effort to reduce the possible contribution of electrophysiologic disturbances in the described areas to psychotic symptoms. When interictal psychosis persists despite such adjustments, initiation with low-dose atypical antipsychotics carries the least risk of lowering seizure threshold and should be considered.

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