Discuss this article at www.facebook.com/CurrentPsychiatry

Alzheimer’s disease (AD) and dementia with Lewy bodies (DLB) are the first and second most common causes of neurodegenerative dementia, respectively.^{“New Alzheimer’s disease guidelines: Implications for clinicians,” Current Psychiatry, March 2012, p. 15-20; http://bit.ly/UNYikk.}

The 2005 report of the DLB Consortium⁵ recognizes central, core, suggestive, and supportive features of DLB (Table 1).^5,10 These features are considered in the context of other confounding clinical conditions and the timing of cognitive and motor symptoms. The revised DLB criteria⁵ require a central feature of progressive cognitive decline. “Probable DLB” is when a patient presents with 2 core features or 1 core feature and ≥1 suggestive features. A diagnosis of “possible DLB” requires 1 core feature or 1 suggestive feature in the presence of progressive cognitive decline.

Table 1

Diagnostic criteria for AD and DLB

Biomarkers for AD, but not DLB

The 2011 diagnostic criteria for AD incorporate biomarkers that can be measured in vivo and reflect speci?c features of disease-related pathophysiologic processes. Biomarkers for AD are divided into 2 categories:¹¹

• amyloid-beta (Aβ) accumulation: abnormal tracer retention on amyloid positron emission topography (PET) imaging and low cerebrospinal fluid (CSF) Aβ42
• neuronal degeneration or injury: elevated CSF tau (total and phosphorylated tau), decreased ?uorodeoxyglucose uptake on PET in temporo-parietal cortices, and atrophy on structural MRI in the hippocampal and temporo-parietal regions.

No clinically applicable genotypic or CSF markers exist to support a DLB diagnosis, but there are many promising candidates, including elevated levels of CSF p-tau 181, CSF levels of alpha- and beta-synuclein,¹² and CSF beta-glucocerebrosidase levels.¹³ PET mapping of brain acetylcholinesterase activity,¹⁴ 123I-2β-carbomethoxy-3β- (4-iodophenyl)-N-(3-fluoropropyl)nortropane single photon emission computed tomography (SPECT) dopamine transporter (DaT) imaging¹⁵ and metaiodobenzylguanidine (MIBG) scintigraphy also are promising methods. DaT scan SPECT is FDA-approved for detecting loss of functional dopaminergic neuron terminals in the striatum and can differentiate between AD and DLB with a sensitivity and specificity of 78% to 88% and 94% to 100%, respectively.¹⁶ This test is covered by Medicare for differentiating AD and DLB.

Differences in presentation

Cognitive impairment. Contrary to the early memory impairment that characterizes AD, memory deficits in DLB usually appear later in the disease course.⁵ Patients with DLB manifest greater attentional, visuospatial, and executive impairments than those with AD, whereas AD causes more profound episodic (declarative) memory impairment than DLB. DLB patients show more preserved consolidation and storage of verbal information than AD patients because of less neuroanatomical and cholinergic compromise in the medial temporal lobe. There is no evidence of significant differences in remote memory, semantic memory, and language (naming and fluency).

Compromised attention in DLB may be the basis for fluctuating cognition, a characteristic of the disease. The greater attentional impairment and reaction time variability in DLB compared with AD is evident during complex tasks for attention and may be a function of the executive and visuospatial demands of the tasks.¹⁷

Executive functions critical to adaptive, goal-directed behavior are more impaired in DLB than AD. DLB patients are more susceptible to distraction and have difficulty engaging in a task and shifting from 1 task to another. This, together with a tendency for confabulation and perseveration, are signs of executive dysfunction.

Neuropsychiatric features. DLB patients are more likely than AD patients to exhibit psychiatric symptoms and have more functional impairment.¹⁸ In an analysis of autopsy-confirmed cases, hallucinations and delusions were more frequent with Lewy body pathology (75%) than AD (21%) at initial clinical evaluation.¹⁸ By the end stages of both illnesses, the degree of psychotic symptoms is comparable.¹⁹ Depression is common in DLB; whether base rates of depressed mood and major depression differ between DLB and AD is uncertain.²⁰

Psychosis in AD can be induced by medication or delirium, or triggered by poor sensory perceptions. Psychotic symptoms occur more frequently during the moderate and advanced stages of AD, when patients present with visual hallucinations, delusions, or delusional misidentifications. As many as 10% to 20% of patients with AD experience hallucinations, typically visual. Delusions occur in 30% to 50% of AD patients, usually in the later stages of the disease. The most common delusional themes are infidelity, theft, and paranoia. Female sex is a risk factor for psychosis in AD. Delusions co-occur with aggression, anxiety, and aberrant motor behavior.

Visual hallucinations—mostly vivid, well-formed, false perceptions of insects, animals, or people—are the defining feature of DLB.²¹ Many patients recognize that they are experiencing visual hallucinations and can ignore them. DLB patients also may experience visual illusions, such as misperceiving household objects as living beings. Delusions—typically paranoid—are common among DLB patients, as are depression and anxiety.¹ Agitation or aggressive behavior tends to occur late in the illness, if at all.

The causes of psychotic symptoms in DLB are not fully understood, but dopamine dysfunction likely is involved in hallucinations, delusions, and agitation, and serotonin dysfunction may be associated with depression and anxiety. Rapid eye movement (REM) sleep/wakefulness dysregulation, in which the dream imagery of REM sleep may occur during wakefulness, also has been proposed as a mechanism for visual hallucinations in DLB.²² In DLB, psychotic symptoms occur early and are a hallmark of this illness, whereas in AD they usually occur in the middle to late stages of the disease.

Motor symptoms. In AD, extrapyramidal symptoms (EPS) are common later in the disease, are strongly correlated with disease severity, and are a strong, independent predictor of depression severity.²³ EPS are more common in DLB than in AD²⁴ and DLB patients are at higher risk of developing EPS even with low doses of typical antipsychotics, compared with AD patients.²⁵

Other symptoms. REM sleep behavior disorder (RBD) is characterized by enacting dreams—often violent—during REM sleep. RBD is common in DLB and many patients also have excessive daytime somnolence. Other sleep disorders in DLB include insomnia, obstructive sleep apnea, central sleep apnea, restless legs syndrome, and periodic limb movements during sleep.

In AD patients, common sleep behaviors include confusion in the early evening (“sundowning”) and frequent nighttime awakenings, often accompanied by wandering.²⁶ Orthostatic hypotension, impotence, urinary incontinence, and constipation are common in DLB. Lack of insight concerning personal cognitive, mood, and behavioral state is highly prevalent in AD patients and more common than in DLB.

Diagnostic evaluation

Because there are no definitive clinical markers for DLB, diagnosis is based on a detailed clinical and family history from the patient and a reliable informant, as well as a physical, neurologic, and mental status examination that looks for associated noncognitive symptoms, and neuropsychological evaluation. Reasons DLB may be misdiagnosed include:

• Some “core” clinical features of DLB may not appear or may overlap with AD.
• Presence and severity of concurrent AD pathology in DLB may modify the clinical presentation, with decreased rates of hallucinations and parkinsonism and increased neurofibrillary tangles.
• Failure to reliably identify fluctuations—variations in cognition and arousal, such as periods of unresponsiveness while awake (“zoning out”), excessive daytime somnolence, and disorganized speech.²⁷

Detecting and characterizing cognitive deficits in dementia patients using neuropsychological testing is important in establishing a clinical diagnosis, determining baseline levels of impairment, forming a prognosis, and initiating disease-specific treatments. Differences in neuropsychological findings in AD and DLB are outlined in Table 2.^16,28-33 Several studies have suggested using these measures to differentiate patients with DLB from those with AD.²⁰

Table 2

Diagnostic testing for Alzheimer’s disease and dementia with Lewy bodies

Evidence is insufficient to support using electroencephalographic and polysomnographic studies when initially evaluating patients with dementia. Brain CT or MRI are recommended as part of the initial evaluation of dementia patients to exclude treatable causes of dementia and help clarify the differential diagnosis. Occipital hypometabolism and hypoperfusion demonstrated on PET and SPECT imaging have high sensitivity and specificity for differentiating AD from DLB.

To diagnose DLB more consistently, look for core features of the disease, RBD, antipsychotic hypersensitivity, and decreased striatal binding at presynaptic DaT sites.¹⁵ Abnormal (low binding) DaT activity is the most reliable diagnostic marker for DLB.³⁴ Myocardial scintigraphy with MIBG is sensitive to pathologic changes of DLB before clinical expression and could overcome the difficulties of using clinical criteria alone to identify patients with DLB.³⁵ MIBG scintigraphy may be preferred to DaT scan because it is less expensive and its sensitivity and specificity to DLB are independent of the presence of parkinsonism.³⁵

For an overview of pharmacotherapy options for patients with AD or DLB, see Box 2.

Box 2

Related Resources

• Hanyu H, Sato T, Hirao K, et al. Differences in clinical course between dementia with Lewy bodies and Alzheimer’s disease. Eur J Neurol. 2009;16(2):212-217.
• Walker Z, McKeith I, Rodda J, et al. Comparison of cognitive decline between dementia with Lewy bodies and Alzheimer’s disease: a cohort study. BMJ Open. 2012;2:e000380.

Drug Brand Names

• Aripiprazole • Abilify
• Clonazepam • Klonopin
• Donepezil • Aricept
• Galantamine • Razadyne, Reminyl
• Levodopa • Dopar, Larodopa
• Memantine • Namenda
• Quetiapine • Seroquel
• Rivastigmine • Exelon

Disclosure

Drs. Bishnoi and Manepalli report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Grossberg serves as a consultant to Forest, Janssen, Novartis, and Pfizer. His department receives research funding from Novartis, Janssen, and Pfizer.

Discuss this article at www.facebook.com/CurrentPsychiatry

Alzheimer’s disease (AD) and dementia with Lewy bodies (DLB) are the first and second most common causes of neurodegenerative dementia, respectively.^{“New Alzheimer’s disease guidelines: Implications for clinicians,” Current Psychiatry, March 2012, p. 15-20; http://bit.ly/UNYikk.}

The 2005 report of the DLB Consortium⁵ recognizes central, core, suggestive, and supportive features of DLB (Table 1).^5,10 These features are considered in the context of other confounding clinical conditions and the timing of cognitive and motor symptoms. The revised DLB criteria⁵ require a central feature of progressive cognitive decline. “Probable DLB” is when a patient presents with 2 core features or 1 core feature and ≥1 suggestive features. A diagnosis of “possible DLB” requires 1 core feature or 1 suggestive feature in the presence of progressive cognitive decline.

Table 1

Diagnostic criteria for AD and DLB

Biomarkers for AD, but not DLB

The 2011 diagnostic criteria for AD incorporate biomarkers that can be measured in vivo and reflect speci?c features of disease-related pathophysiologic processes. Biomarkers for AD are divided into 2 categories:¹¹

• amyloid-beta (Aβ) accumulation: abnormal tracer retention on amyloid positron emission topography (PET) imaging and low cerebrospinal fluid (CSF) Aβ42
• neuronal degeneration or injury: elevated CSF tau (total and phosphorylated tau), decreased ?uorodeoxyglucose uptake on PET in temporo-parietal cortices, and atrophy on structural MRI in the hippocampal and temporo-parietal regions.

No clinically applicable genotypic or CSF markers exist to support a DLB diagnosis, but there are many promising candidates, including elevated levels of CSF p-tau 181, CSF levels of alpha- and beta-synuclein,¹² and CSF beta-glucocerebrosidase levels.¹³ PET mapping of brain acetylcholinesterase activity,¹⁴ 123I-2β-carbomethoxy-3β- (4-iodophenyl)-N-(3-fluoropropyl)nortropane single photon emission computed tomography (SPECT) dopamine transporter (DaT) imaging¹⁵ and metaiodobenzylguanidine (MIBG) scintigraphy also are promising methods. DaT scan SPECT is FDA-approved for detecting loss of functional dopaminergic neuron terminals in the striatum and can differentiate between AD and DLB with a sensitivity and specificity of 78% to 88% and 94% to 100%, respectively.¹⁶ This test is covered by Medicare for differentiating AD and DLB.

Differences in presentation

Cognitive impairment. Contrary to the early memory impairment that characterizes AD, memory deficits in DLB usually appear later in the disease course.⁵ Patients with DLB manifest greater attentional, visuospatial, and executive impairments than those with AD, whereas AD causes more profound episodic (declarative) memory impairment than DLB. DLB patients show more preserved consolidation and storage of verbal information than AD patients because of less neuroanatomical and cholinergic compromise in the medial temporal lobe. There is no evidence of significant differences in remote memory, semantic memory, and language (naming and fluency).

Compromised attention in DLB may be the basis for fluctuating cognition, a characteristic of the disease. The greater attentional impairment and reaction time variability in DLB compared with AD is evident during complex tasks for attention and may be a function of the executive and visuospatial demands of the tasks.¹⁷

Executive functions critical to adaptive, goal-directed behavior are more impaired in DLB than AD. DLB patients are more susceptible to distraction and have difficulty engaging in a task and shifting from 1 task to another. This, together with a tendency for confabulation and perseveration, are signs of executive dysfunction.

Neuropsychiatric features. DLB patients are more likely than AD patients to exhibit psychiatric symptoms and have more functional impairment.¹⁸ In an analysis of autopsy-confirmed cases, hallucinations and delusions were more frequent with Lewy body pathology (75%) than AD (21%) at initial clinical evaluation.¹⁸ By the end stages of both illnesses, the degree of psychotic symptoms is comparable.¹⁹ Depression is common in DLB; whether base rates of depressed mood and major depression differ between DLB and AD is uncertain.²⁰

Psychosis in AD can be induced by medication or delirium, or triggered by poor sensory perceptions. Psychotic symptoms occur more frequently during the moderate and advanced stages of AD, when patients present with visual hallucinations, delusions, or delusional misidentifications. As many as 10% to 20% of patients with AD experience hallucinations, typically visual. Delusions occur in 30% to 50% of AD patients, usually in the later stages of the disease. The most common delusional themes are infidelity, theft, and paranoia. Female sex is a risk factor for psychosis in AD. Delusions co-occur with aggression, anxiety, and aberrant motor behavior.

Visual hallucinations—mostly vivid, well-formed, false perceptions of insects, animals, or people—are the defining feature of DLB.²¹ Many patients recognize that they are experiencing visual hallucinations and can ignore them. DLB patients also may experience visual illusions, such as misperceiving household objects as living beings. Delusions—typically paranoid—are common among DLB patients, as are depression and anxiety.¹ Agitation or aggressive behavior tends to occur late in the illness, if at all.

The causes of psychotic symptoms in DLB are not fully understood, but dopamine dysfunction likely is involved in hallucinations, delusions, and agitation, and serotonin dysfunction may be associated with depression and anxiety. Rapid eye movement (REM) sleep/wakefulness dysregulation, in which the dream imagery of REM sleep may occur during wakefulness, also has been proposed as a mechanism for visual hallucinations in DLB.²² In DLB, psychotic symptoms occur early and are a hallmark of this illness, whereas in AD they usually occur in the middle to late stages of the disease.

Motor symptoms. In AD, extrapyramidal symptoms (EPS) are common later in the disease, are strongly correlated with disease severity, and are a strong, independent predictor of depression severity.²³ EPS are more common in DLB than in AD²⁴ and DLB patients are at higher risk of developing EPS even with low doses of typical antipsychotics, compared with AD patients.²⁵

Other symptoms. REM sleep behavior disorder (RBD) is characterized by enacting dreams—often violent—during REM sleep. RBD is common in DLB and many patients also have excessive daytime somnolence. Other sleep disorders in DLB include insomnia, obstructive sleep apnea, central sleep apnea, restless legs syndrome, and periodic limb movements during sleep.

In AD patients, common sleep behaviors include confusion in the early evening (“sundowning”) and frequent nighttime awakenings, often accompanied by wandering.²⁶ Orthostatic hypotension, impotence, urinary incontinence, and constipation are common in DLB. Lack of insight concerning personal cognitive, mood, and behavioral state is highly prevalent in AD patients and more common than in DLB.

Diagnostic evaluation

Because there are no definitive clinical markers for DLB, diagnosis is based on a detailed clinical and family history from the patient and a reliable informant, as well as a physical, neurologic, and mental status examination that looks for associated noncognitive symptoms, and neuropsychological evaluation. Reasons DLB may be misdiagnosed include:

• Some “core” clinical features of DLB may not appear or may overlap with AD.
• Presence and severity of concurrent AD pathology in DLB may modify the clinical presentation, with decreased rates of hallucinations and parkinsonism and increased neurofibrillary tangles.
• Failure to reliably identify fluctuations—variations in cognition and arousal, such as periods of unresponsiveness while awake (“zoning out”), excessive daytime somnolence, and disorganized speech.²⁷

Detecting and characterizing cognitive deficits in dementia patients using neuropsychological testing is important in establishing a clinical diagnosis, determining baseline levels of impairment, forming a prognosis, and initiating disease-specific treatments. Differences in neuropsychological findings in AD and DLB are outlined in Table 2.^16,28-33 Several studies have suggested using these measures to differentiate patients with DLB from those with AD.²⁰

Table 2

Diagnostic testing for Alzheimer’s disease and dementia with Lewy bodies

Evidence is insufficient to support using electroencephalographic and polysomnographic studies when initially evaluating patients with dementia. Brain CT or MRI are recommended as part of the initial evaluation of dementia patients to exclude treatable causes of dementia and help clarify the differential diagnosis. Occipital hypometabolism and hypoperfusion demonstrated on PET and SPECT imaging have high sensitivity and specificity for differentiating AD from DLB.

To diagnose DLB more consistently, look for core features of the disease, RBD, antipsychotic hypersensitivity, and decreased striatal binding at presynaptic DaT sites.¹⁵ Abnormal (low binding) DaT activity is the most reliable diagnostic marker for DLB.³⁴ Myocardial scintigraphy with MIBG is sensitive to pathologic changes of DLB before clinical expression and could overcome the difficulties of using clinical criteria alone to identify patients with DLB.³⁵ MIBG scintigraphy may be preferred to DaT scan because it is less expensive and its sensitivity and specificity to DLB are independent of the presence of parkinsonism.³⁵

For an overview of pharmacotherapy options for patients with AD or DLB, see Box 2.

Box 2

Related Resources

• Hanyu H, Sato T, Hirao K, et al. Differences in clinical course between dementia with Lewy bodies and Alzheimer’s disease. Eur J Neurol. 2009;16(2):212-217.
• Walker Z, McKeith I, Rodda J, et al. Comparison of cognitive decline between dementia with Lewy bodies and Alzheimer’s disease: a cohort study. BMJ Open. 2012;2:e000380.

Drug Brand Names

• Aripiprazole • Abilify
• Clonazepam • Klonopin
• Donepezil • Aricept
• Galantamine • Razadyne, Reminyl
• Levodopa • Dopar, Larodopa
• Memantine • Namenda
• Quetiapine • Seroquel
• Rivastigmine • Exelon

Disclosure

Drs. Bishnoi and Manepalli report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Grossberg serves as a consultant to Forest, Janssen, Novartis, and Pfizer. His department receives research funding from Novartis, Janssen, and Pfizer.

Discuss this article at www.facebook.com/CurrentPsychiatry

Alzheimer’s disease (AD) and dementia with Lewy bodies (DLB) are the first and second most common causes of neurodegenerative dementia, respectively.^{“New Alzheimer’s disease guidelines: Implications for clinicians,” Current Psychiatry, March 2012, p. 15-20; http://bit.ly/UNYikk.}

The 2005 report of the DLB Consortium⁵ recognizes central, core, suggestive, and supportive features of DLB (Table 1).^5,10 These features are considered in the context of other confounding clinical conditions and the timing of cognitive and motor symptoms. The revised DLB criteria⁵ require a central feature of progressive cognitive decline. “Probable DLB” is when a patient presents with 2 core features or 1 core feature and ≥1 suggestive features. A diagnosis of “possible DLB” requires 1 core feature or 1 suggestive feature in the presence of progressive cognitive decline.

Table 1

Diagnostic criteria for AD and DLB

Biomarkers for AD, but not DLB

The 2011 diagnostic criteria for AD incorporate biomarkers that can be measured in vivo and reflect speci?c features of disease-related pathophysiologic processes. Biomarkers for AD are divided into 2 categories:¹¹

• amyloid-beta (Aβ) accumulation: abnormal tracer retention on amyloid positron emission topography (PET) imaging and low cerebrospinal fluid (CSF) Aβ42
• neuronal degeneration or injury: elevated CSF tau (total and phosphorylated tau), decreased ?uorodeoxyglucose uptake on PET in temporo-parietal cortices, and atrophy on structural MRI in the hippocampal and temporo-parietal regions.

No clinically applicable genotypic or CSF markers exist to support a DLB diagnosis, but there are many promising candidates, including elevated levels of CSF p-tau 181, CSF levels of alpha- and beta-synuclein,¹² and CSF beta-glucocerebrosidase levels.¹³ PET mapping of brain acetylcholinesterase activity,¹⁴ 123I-2β-carbomethoxy-3β- (4-iodophenyl)-N-(3-fluoropropyl)nortropane single photon emission computed tomography (SPECT) dopamine transporter (DaT) imaging¹⁵ and metaiodobenzylguanidine (MIBG) scintigraphy also are promising methods. DaT scan SPECT is FDA-approved for detecting loss of functional dopaminergic neuron terminals in the striatum and can differentiate between AD and DLB with a sensitivity and specificity of 78% to 88% and 94% to 100%, respectively.¹⁶ This test is covered by Medicare for differentiating AD and DLB.

Differences in presentation

Cognitive impairment. Contrary to the early memory impairment that characterizes AD, memory deficits in DLB usually appear later in the disease course.⁵ Patients with DLB manifest greater attentional, visuospatial, and executive impairments than those with AD, whereas AD causes more profound episodic (declarative) memory impairment than DLB. DLB patients show more preserved consolidation and storage of verbal information than AD patients because of less neuroanatomical and cholinergic compromise in the medial temporal lobe. There is no evidence of significant differences in remote memory, semantic memory, and language (naming and fluency).

Compromised attention in DLB may be the basis for fluctuating cognition, a characteristic of the disease. The greater attentional impairment and reaction time variability in DLB compared with AD is evident during complex tasks for attention and may be a function of the executive and visuospatial demands of the tasks.¹⁷

Executive functions critical to adaptive, goal-directed behavior are more impaired in DLB than AD. DLB patients are more susceptible to distraction and have difficulty engaging in a task and shifting from 1 task to another. This, together with a tendency for confabulation and perseveration, are signs of executive dysfunction.

Neuropsychiatric features. DLB patients are more likely than AD patients to exhibit psychiatric symptoms and have more functional impairment.¹⁸ In an analysis of autopsy-confirmed cases, hallucinations and delusions were more frequent with Lewy body pathology (75%) than AD (21%) at initial clinical evaluation.¹⁸ By the end stages of both illnesses, the degree of psychotic symptoms is comparable.¹⁹ Depression is common in DLB; whether base rates of depressed mood and major depression differ between DLB and AD is uncertain.²⁰

Psychosis in AD can be induced by medication or delirium, or triggered by poor sensory perceptions. Psychotic symptoms occur more frequently during the moderate and advanced stages of AD, when patients present with visual hallucinations, delusions, or delusional misidentifications. As many as 10% to 20% of patients with AD experience hallucinations, typically visual. Delusions occur in 30% to 50% of AD patients, usually in the later stages of the disease. The most common delusional themes are infidelity, theft, and paranoia. Female sex is a risk factor for psychosis in AD. Delusions co-occur with aggression, anxiety, and aberrant motor behavior.

Visual hallucinations—mostly vivid, well-formed, false perceptions of insects, animals, or people—are the defining feature of DLB.²¹ Many patients recognize that they are experiencing visual hallucinations and can ignore them. DLB patients also may experience visual illusions, such as misperceiving household objects as living beings. Delusions—typically paranoid—are common among DLB patients, as are depression and anxiety.¹ Agitation or aggressive behavior tends to occur late in the illness, if at all.

The causes of psychotic symptoms in DLB are not fully understood, but dopamine dysfunction likely is involved in hallucinations, delusions, and agitation, and serotonin dysfunction may be associated with depression and anxiety. Rapid eye movement (REM) sleep/wakefulness dysregulation, in which the dream imagery of REM sleep may occur during wakefulness, also has been proposed as a mechanism for visual hallucinations in DLB.²² In DLB, psychotic symptoms occur early and are a hallmark of this illness, whereas in AD they usually occur in the middle to late stages of the disease.

Motor symptoms. In AD, extrapyramidal symptoms (EPS) are common later in the disease, are strongly correlated with disease severity, and are a strong, independent predictor of depression severity.²³ EPS are more common in DLB than in AD²⁴ and DLB patients are at higher risk of developing EPS even with low doses of typical antipsychotics, compared with AD patients.²⁵

Other symptoms. REM sleep behavior disorder (RBD) is characterized by enacting dreams—often violent—during REM sleep. RBD is common in DLB and many patients also have excessive daytime somnolence. Other sleep disorders in DLB include insomnia, obstructive sleep apnea, central sleep apnea, restless legs syndrome, and periodic limb movements during sleep.

In AD patients, common sleep behaviors include confusion in the early evening (“sundowning”) and frequent nighttime awakenings, often accompanied by wandering.²⁶ Orthostatic hypotension, impotence, urinary incontinence, and constipation are common in DLB. Lack of insight concerning personal cognitive, mood, and behavioral state is highly prevalent in AD patients and more common than in DLB.

Diagnostic evaluation

Because there are no definitive clinical markers for DLB, diagnosis is based on a detailed clinical and family history from the patient and a reliable informant, as well as a physical, neurologic, and mental status examination that looks for associated noncognitive symptoms, and neuropsychological evaluation. Reasons DLB may be misdiagnosed include:

• Some “core” clinical features of DLB may not appear or may overlap with AD.
• Presence and severity of concurrent AD pathology in DLB may modify the clinical presentation, with decreased rates of hallucinations and parkinsonism and increased neurofibrillary tangles.
• Failure to reliably identify fluctuations—variations in cognition and arousal, such as periods of unresponsiveness while awake (“zoning out”), excessive daytime somnolence, and disorganized speech.²⁷

Detecting and characterizing cognitive deficits in dementia patients using neuropsychological testing is important in establishing a clinical diagnosis, determining baseline levels of impairment, forming a prognosis, and initiating disease-specific treatments. Differences in neuropsychological findings in AD and DLB are outlined in Table 2.^16,28-33 Several studies have suggested using these measures to differentiate patients with DLB from those with AD.²⁰

Table 2

Diagnostic testing for Alzheimer’s disease and dementia with Lewy bodies

Evidence is insufficient to support using electroencephalographic and polysomnographic studies when initially evaluating patients with dementia. Brain CT or MRI are recommended as part of the initial evaluation of dementia patients to exclude treatable causes of dementia and help clarify the differential diagnosis. Occipital hypometabolism and hypoperfusion demonstrated on PET and SPECT imaging have high sensitivity and specificity for differentiating AD from DLB.

To diagnose DLB more consistently, look for core features of the disease, RBD, antipsychotic hypersensitivity, and decreased striatal binding at presynaptic DaT sites.¹⁵ Abnormal (low binding) DaT activity is the most reliable diagnostic marker for DLB.³⁴ Myocardial scintigraphy with MIBG is sensitive to pathologic changes of DLB before clinical expression and could overcome the difficulties of using clinical criteria alone to identify patients with DLB.³⁵ MIBG scintigraphy may be preferred to DaT scan because it is less expensive and its sensitivity and specificity to DLB are independent of the presence of parkinsonism.³⁵

For an overview of pharmacotherapy options for patients with AD or DLB, see Box 2.

Box 2

Related Resources

• Hanyu H, Sato T, Hirao K, et al. Differences in clinical course between dementia with Lewy bodies and Alzheimer’s disease. Eur J Neurol. 2009;16(2):212-217.
• Walker Z, McKeith I, Rodda J, et al. Comparison of cognitive decline between dementia with Lewy bodies and Alzheimer’s disease: a cohort study. BMJ Open. 2012;2:e000380.

Drug Brand Names

• Aripiprazole • Abilify
• Clonazepam • Klonopin
• Donepezil • Aricept
• Galantamine • Razadyne, Reminyl
• Levodopa • Dopar, Larodopa
• Memantine • Namenda
• Quetiapine • Seroquel
• Rivastigmine • Exelon

Disclosure

Drs. Bishnoi and Manepalli report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Grossberg serves as a consultant to Forest, Janssen, Novartis, and Pfizer. His department receives research funding from Novartis, Janssen, and Pfizer.

Despite the widespread dissemination of information about the health risks associated with smoking, many cancer patients continue to smoke, which results in a decreased quality of life, an increased probability of cancer recurrence, and a decreased survival time. Efficacious interventions are available to assist cancer patients to quit smoking, yet smoking cessation interventions are often not implemented. This review describes how clinicians, administrators, insurers, and purchasers can encourage a culture of health care in which tobacco cessation interventions are implemented consistent with evidence-based standards of care. Implementing efficacious tobacco cessation interventions can reduce morbidity and mortality among cancer patients...

*Click on the link to the left of this introduction for a PDF of the full article.  

Despite the widespread dissemination of information about the health risks associated with smoking, many cancer patients continue to smoke, which results in a decreased quality of life, an increased probability of cancer recurrence, and a decreased survival time. Efficacious interventions are available to assist cancer patients to quit smoking, yet smoking cessation interventions are often not implemented. This review describes how clinicians, administrators, insurers, and purchasers can encourage a culture of health care in which tobacco cessation interventions are implemented consistent with evidence-based standards of care. Implementing efficacious tobacco cessation interventions can reduce morbidity and mortality among cancer patients...

*Click on the link to the left of this introduction for a PDF of the full article.  

Despite the widespread dissemination of information about the health risks associated with smoking, many cancer patients continue to smoke, which results in a decreased quality of life, an increased probability of cancer recurrence, and a decreased survival time. Efficacious interventions are available to assist cancer patients to quit smoking, yet smoking cessation interventions are often not implemented. This review describes how clinicians, administrators, insurers, and purchasers can encourage a culture of health care in which tobacco cessation interventions are implemented consistent with evidence-based standards of care. Implementing efficacious tobacco cessation interventions can reduce morbidity and mortality among cancer patients...

*Click on the link to the left of this introduction for a PDF of the full article.  

Dasatinib has been approved for first-line treatment of chronic-phase chronic myeloid leukemia by the Food and Drug Administration and is recommended as a first-line treatment option by the National Comprehensive Cancer Network. Based on in vitro data, dasatinib seems to be less susceptible to the resistance mechanisms that affect imatinib. Dasatinib is an effective second-line treatment in patients who are resistant to imatinib. First-line clinical data show that dasatinib provides more rapid and deeper degrees of response than does imatinib, which may correlate with improvements in long-term patient outcome. Grade 1 or 2 cytopenias are the most common adverse events of first-line dasatinib treatment. In a phase 3 comparison with imatinib, several types of nonhematologic adverse events were less frequent in the dasatinib arm; frequencies of grade 3 and 4 events were   2%. Among patients with a minimum follow-up of 24 months, grade 1 or 2 pleural effusion was reported in 14% of dasatinib-treated patients and was manageable in almost all cases; no grade 3 or 4 pleural effusion occurred. Prompt and effective monitoring and management of dasatinib toxicities is essential to minimize intolerance and nonadherence to therapy. Patient education is important to increase the likelihood of prompt management and provide reassurance. Recommendations for patient monitoring, management, and education are provided.

*For a PDF of the full article, click on the link to the left of this introduction.

Dasatinib has been approved for first-line treatment of chronic-phase chronic myeloid leukemia by the Food and Drug Administration and is recommended as a first-line treatment option by the National Comprehensive Cancer Network. Based on in vitro data, dasatinib seems to be less susceptible to the resistance mechanisms that affect imatinib. Dasatinib is an effective second-line treatment in patients who are resistant to imatinib. First-line clinical data show that dasatinib provides more rapid and deeper degrees of response than does imatinib, which may correlate with improvements in long-term patient outcome. Grade 1 or 2 cytopenias are the most common adverse events of first-line dasatinib treatment. In a phase 3 comparison with imatinib, several types of nonhematologic adverse events were less frequent in the dasatinib arm; frequencies of grade 3 and 4 events were   2%. Among patients with a minimum follow-up of 24 months, grade 1 or 2 pleural effusion was reported in 14% of dasatinib-treated patients and was manageable in almost all cases; no grade 3 or 4 pleural effusion occurred. Prompt and effective monitoring and management of dasatinib toxicities is essential to minimize intolerance and nonadherence to therapy. Patient education is important to increase the likelihood of prompt management and provide reassurance. Recommendations for patient monitoring, management, and education are provided.

*For a PDF of the full article, click on the link to the left of this introduction.

Dasatinib has been approved for first-line treatment of chronic-phase chronic myeloid leukemia by the Food and Drug Administration and is recommended as a first-line treatment option by the National Comprehensive Cancer Network. Based on in vitro data, dasatinib seems to be less susceptible to the resistance mechanisms that affect imatinib. Dasatinib is an effective second-line treatment in patients who are resistant to imatinib. First-line clinical data show that dasatinib provides more rapid and deeper degrees of response than does imatinib, which may correlate with improvements in long-term patient outcome. Grade 1 or 2 cytopenias are the most common adverse events of first-line dasatinib treatment. In a phase 3 comparison with imatinib, several types of nonhematologic adverse events were less frequent in the dasatinib arm; frequencies of grade 3 and 4 events were   2%. Among patients with a minimum follow-up of 24 months, grade 1 or 2 pleural effusion was reported in 14% of dasatinib-treated patients and was manageable in almost all cases; no grade 3 or 4 pleural effusion occurred. Prompt and effective monitoring and management of dasatinib toxicities is essential to minimize intolerance and nonadherence to therapy. Patient education is important to increase the likelihood of prompt management and provide reassurance. Recommendations for patient monitoring, management, and education are provided.

*For a PDF of the full article, click on the link to the left of this introduction.

A national outbreak of fungal meningitis tied to contaminated steroids in epidural injections should make hospitalists vigilant with patients who present potential symptoms, says an infectious-disease (ID) specialist.

Earlier this month, health officials linked the outbreak to tainted batches of steroids used in spinal injections, and they say it could be weeks, or even months, before they know whether the incubation period for the disease is over, according to The New York Times.

"The key in my mind is that hospitalists ought to have a high index of suspicion for this right now," says hospitalist and ID expert James Pile, MD, FACP, SFHM, of the Cleveland Clinic. "If you encounter a patient you think may have meningitis, may have a brain stem stroke, may have an epidural abscess or vertebral osteomyelitis...at least think and ask the patient, or their family member, 'Did you receive an epidural steroid injection recently?'"

The answer to that question will help determine the best care delivery for hospitalists, and physicians should not rely on patients to relay the information without being asked for it, Dr. Pile says.

The outbreak has been traced to three contaminated batches of methylprednisolone produced by the New England Compounding Center in Framingham, Mass. The company, which is under criminal investigation, has been linked to at least 25 deaths and more than 317 infected patients. Although 14,000 people might have been injected with the contaminated compound, CDC officials say the likelihood of infection remains relatively low.

Dr. Pile says that while hospitalists might see only a handful of fungal meningitis cases in their careers, they still need to keep the possibility in mind when examining patients. It's a safe approach to take, particularly as the CDC continues to investigate the extent of the outbreak. The CDC has advised against antifungal prophylaxis or presumptive treatment of exposed asymptomatic patients without a diagnosed case of meningitis.

"This is just unfolding so quickly, it's a moving target," Dr. Pile adds. "How big it ends up being and what kinds of new or unusual manifestations present remain to be seen."

Visit our website for more information about infectious disease and hospital medicine.

A national outbreak of fungal meningitis tied to contaminated steroids in epidural injections should make hospitalists vigilant with patients who present potential symptoms, says an infectious-disease (ID) specialist.

Earlier this month, health officials linked the outbreak to tainted batches of steroids used in spinal injections, and they say it could be weeks, or even months, before they know whether the incubation period for the disease is over, according to The New York Times.

"The key in my mind is that hospitalists ought to have a high index of suspicion for this right now," says hospitalist and ID expert James Pile, MD, FACP, SFHM, of the Cleveland Clinic. "If you encounter a patient you think may have meningitis, may have a brain stem stroke, may have an epidural abscess or vertebral osteomyelitis...at least think and ask the patient, or their family member, 'Did you receive an epidural steroid injection recently?'"

The answer to that question will help determine the best care delivery for hospitalists, and physicians should not rely on patients to relay the information without being asked for it, Dr. Pile says.

The outbreak has been traced to three contaminated batches of methylprednisolone produced by the New England Compounding Center in Framingham, Mass. The company, which is under criminal investigation, has been linked to at least 25 deaths and more than 317 infected patients. Although 14,000 people might have been injected with the contaminated compound, CDC officials say the likelihood of infection remains relatively low.

Dr. Pile says that while hospitalists might see only a handful of fungal meningitis cases in their careers, they still need to keep the possibility in mind when examining patients. It's a safe approach to take, particularly as the CDC continues to investigate the extent of the outbreak. The CDC has advised against antifungal prophylaxis or presumptive treatment of exposed asymptomatic patients without a diagnosed case of meningitis.

"This is just unfolding so quickly, it's a moving target," Dr. Pile adds. "How big it ends up being and what kinds of new or unusual manifestations present remain to be seen."

Visit our website for more information about infectious disease and hospital medicine.

A national outbreak of fungal meningitis tied to contaminated steroids in epidural injections should make hospitalists vigilant with patients who present potential symptoms, says an infectious-disease (ID) specialist.

Earlier this month, health officials linked the outbreak to tainted batches of steroids used in spinal injections, and they say it could be weeks, or even months, before they know whether the incubation period for the disease is over, according to The New York Times.

"The key in my mind is that hospitalists ought to have a high index of suspicion for this right now," says hospitalist and ID expert James Pile, MD, FACP, SFHM, of the Cleveland Clinic. "If you encounter a patient you think may have meningitis, may have a brain stem stroke, may have an epidural abscess or vertebral osteomyelitis...at least think and ask the patient, or their family member, 'Did you receive an epidural steroid injection recently?'"

The answer to that question will help determine the best care delivery for hospitalists, and physicians should not rely on patients to relay the information without being asked for it, Dr. Pile says.

The outbreak has been traced to three contaminated batches of methylprednisolone produced by the New England Compounding Center in Framingham, Mass. The company, which is under criminal investigation, has been linked to at least 25 deaths and more than 317 infected patients. Although 14,000 people might have been injected with the contaminated compound, CDC officials say the likelihood of infection remains relatively low.

Dr. Pile says that while hospitalists might see only a handful of fungal meningitis cases in their careers, they still need to keep the possibility in mind when examining patients. It's a safe approach to take, particularly as the CDC continues to investigate the extent of the outbreak. The CDC has advised against antifungal prophylaxis or presumptive treatment of exposed asymptomatic patients without a diagnosed case of meningitis.

"This is just unfolding so quickly, it's a moving target," Dr. Pile adds. "How big it ends up being and what kinds of new or unusual manifestations present remain to be seen."

Visit our website for more information about infectious disease and hospital medicine.

The largest effort to date to tackle central-line-associated bloodstream infections (CLABSIs) has reduced infection rates in ICUs nationwide by 40%, according to preliminary findings from the federal Agency for Healthcare Research and Quality (AHRQ).

AHRQ attributes the decrease to a CLABSI safety checklist from the Comprehensive Unit-Based Safety Program (CUSP) that encourages hospital staff to wash their hands prior to inserting central lines, avoid the femoral site, remove lines when they are no longer needed, and use the antimicrobial agent chlorhexidine to clean the patient's insertion site.

The checklist was developed by Peter Pronovost, MD, PhD, FCCM, and colleagues at Johns Hopkins University in Baltimore, and originally implemented in ICUs statewide in Michigan as the Keystone Project. Since 2009, CUSP has recruited more than 1,000 participating hospitals in 44 states. CUSP collectively reported a decrease to 1.25 from 1.87 CLABSIs per 1,000 central-line days 10-12 months after implementing the program, according to AHRQ [PDF].

The real game-changer for CLABSIs has been the widespread adoption of chlorhexidine as an insertion site disinfectant, says Sanjay Saint, MD, MPH, director of the Veterans Administration at the University of Michigan Patient Safety Enhancement Program in Ann Arbor and professor of medicine at the University of Michigan. Dr. Saint is on the national leadership team of On the CUSP: Stop CAUTI (Catheter-Associated Urinary Tract Infections), an initiative that aims to reduce mean rates of CAUTI infections by 25% in hospitals nationwide.

Although hospitalists don't routinely place central lines, their role in this procedure is growing, both in nonacademic hospitals that lack intensivists and on hospitals' general medicine floors.

"My take-home message for hospitalists: if you are putting in central lines, if you only make one change in practice, is to use chlorhexidine as the site disinfectant," Dr. Saint says.

Visit our website for more information about central-line-associated bloodstream infections.

The largest effort to date to tackle central-line-associated bloodstream infections (CLABSIs) has reduced infection rates in ICUs nationwide by 40%, according to preliminary findings from the federal Agency for Healthcare Research and Quality (AHRQ).

AHRQ attributes the decrease to a CLABSI safety checklist from the Comprehensive Unit-Based Safety Program (CUSP) that encourages hospital staff to wash their hands prior to inserting central lines, avoid the femoral site, remove lines when they are no longer needed, and use the antimicrobial agent chlorhexidine to clean the patient's insertion site.

The checklist was developed by Peter Pronovost, MD, PhD, FCCM, and colleagues at Johns Hopkins University in Baltimore, and originally implemented in ICUs statewide in Michigan as the Keystone Project. Since 2009, CUSP has recruited more than 1,000 participating hospitals in 44 states. CUSP collectively reported a decrease to 1.25 from 1.87 CLABSIs per 1,000 central-line days 10-12 months after implementing the program, according to AHRQ [PDF].

The real game-changer for CLABSIs has been the widespread adoption of chlorhexidine as an insertion site disinfectant, says Sanjay Saint, MD, MPH, director of the Veterans Administration at the University of Michigan Patient Safety Enhancement Program in Ann Arbor and professor of medicine at the University of Michigan. Dr. Saint is on the national leadership team of On the CUSP: Stop CAUTI (Catheter-Associated Urinary Tract Infections), an initiative that aims to reduce mean rates of CAUTI infections by 25% in hospitals nationwide.

Although hospitalists don't routinely place central lines, their role in this procedure is growing, both in nonacademic hospitals that lack intensivists and on hospitals' general medicine floors.

"My take-home message for hospitalists: if you are putting in central lines, if you only make one change in practice, is to use chlorhexidine as the site disinfectant," Dr. Saint says.

Visit our website for more information about central-line-associated bloodstream infections.

The largest effort to date to tackle central-line-associated bloodstream infections (CLABSIs) has reduced infection rates in ICUs nationwide by 40%, according to preliminary findings from the federal Agency for Healthcare Research and Quality (AHRQ).

AHRQ attributes the decrease to a CLABSI safety checklist from the Comprehensive Unit-Based Safety Program (CUSP) that encourages hospital staff to wash their hands prior to inserting central lines, avoid the femoral site, remove lines when they are no longer needed, and use the antimicrobial agent chlorhexidine to clean the patient's insertion site.

The checklist was developed by Peter Pronovost, MD, PhD, FCCM, and colleagues at Johns Hopkins University in Baltimore, and originally implemented in ICUs statewide in Michigan as the Keystone Project. Since 2009, CUSP has recruited more than 1,000 participating hospitals in 44 states. CUSP collectively reported a decrease to 1.25 from 1.87 CLABSIs per 1,000 central-line days 10-12 months after implementing the program, according to AHRQ [PDF].

The real game-changer for CLABSIs has been the widespread adoption of chlorhexidine as an insertion site disinfectant, says Sanjay Saint, MD, MPH, director of the Veterans Administration at the University of Michigan Patient Safety Enhancement Program in Ann Arbor and professor of medicine at the University of Michigan. Dr. Saint is on the national leadership team of On the CUSP: Stop CAUTI (Catheter-Associated Urinary Tract Infections), an initiative that aims to reduce mean rates of CAUTI infections by 25% in hospitals nationwide.

Although hospitalists don't routinely place central lines, their role in this procedure is growing, both in nonacademic hospitals that lack intensivists and on hospitals' general medicine floors.

"My take-home message for hospitalists: if you are putting in central lines, if you only make one change in practice, is to use chlorhexidine as the site disinfectant," Dr. Saint says.

Visit our website for more information about central-line-associated bloodstream infections.

Adults in Norway with diffuse low-grade gliomas who were treated at a hospital advocating early surgical resection had better overall survival than those treated at a hospital advocating "watchful waiting," according to a report published online Oct. 30 in JAMA.

This finding significantly strengthens the sparse evidence in support of early resection for newly diagnosed diffuse low-grade gliomas, said Dr. Asgeir S. Jakola of the department of neurosurgery, St. Olav’s University Hospital, Trondheim (Norway) and his associates.

Management of these tumors is one of the major controversies in both neurology and oncology today, largely because the effect of surgery on survival is still unclear. The only evidence available until now was based solely on uncontrolled surgical series; some of these have reported that it is safe to withhold surgery until the lesions progress, while others have reported that immediate resection improves survival and delays the time to malignant transformation.

Both patients and physicians are reluctant to undertake immediate surgery when the evidence supporting that strategy has been so tenuous. They also are concerned that the risk of early and aggressive surgery outweighs the benefit, particularly when most patients are capable of normal activity and have a reasonably long life expectancy at diagnosis, the investigators said.

It is unlikely that a randomized, controlled study comparing the two approaches will ever be performed. Dr. Jakola and his colleagues therefore conducted a retrospective, population-based parallel-cohort study at two neurosurgical centers, each of which preferred one of these strategies over the other. Their "natural experiment" was possible because in Norway, there were two such facilities that were relatively close geographically and served a homogenous population. The nationalized health care system distributes training, resources, and personnel equally throughout the country, so the two hospitals were quite similar in other respects. And patient follow-up is 100%.

The 12-year study involved 153 adults with diffuse, histologically verified supratentorial grade I and II tumors diagnosed in 1998-2009, who were followed until death or until April 2011. The median follow-up was 7 years. Gliomas included astrocytomas, oligodendrogliomas, and oligoastrocytomas.

For patients with newly diagnosed low-grade gliomas, hospital A favored biopsy and watchful waiting. The 66 patients treated there typically were followed with MRI at 3 and 6 months, then yearly thereafter. They usually were offered surgical resection, if the lesions grew or showed signs of malignant transformation.

Hospital B favored immediate maximal safe tumor resection for the 87 patients treated there, with MRI follow-up at 6 and 12 months, then annually thereafter. This strategy was not pursued in some patients, however: notably, those who were elderly or had comorbidities and were likely to die from another cause before malignant transformation would take place, and those who had very widespread tumor infiltration that made resection impractical.

The two study groups were well balanced with regard to patient age and comorbidities, and rates of surgical rescue therapy were the same. There also were no differences between the two groups in complications or acquired neurologic deficits.

At the end of the study period, 34 patients (52%) from hospital A had died, compared with only 28 patients (32%) from hospital B. Median survival was 5.9 years at hospital A, but median survival had not yet been reached at hospital B, the researchers said (JAMA 2012;308: [doi:10.1001/jama.2012.12807]).

This survival advantage increased over time. Expected 3-year survival was 70% at hospital A vs. 80% at hospital B; expected 5-year survival was 60% at hospital A vs. 74% at hospital B; and expected 7-year survival was 44% at hospital A vs. 68% at hospital B.

In a post hoc analysis that attempted to account for differences between the two study groups in prognostic factors, the survival benefit for immediate resection remained robust. It also remained robust in another post hoc analysis that examined the subgroup of patients who had the most common glioma, a grade II astrocytoma. Median survival was 5.6 years at the hospital favoring watchful waiting, compared with 9.7 years at the hospital favoring early resection, in this large subgroup of patients.

Based on these findings, hospital A has changed its preferred strategy from watchful waiting to early resection, Dr. Jakola and his associates said.

"Despite the clear survival advantage seen, clinical judgment is still necessary in individual patients with suspected low-grade glioma since results will depend on patient and disease characteristics together with surgical results in terms of resection grades and complication rates," they added.

One of Dr. Jakola’s associates reported holding stock in Sonowand, manufacturer of the 3-D ultrasound-based imaging system used in one of the study hospitals.

Adults in Norway with diffuse low-grade gliomas who were treated at a hospital advocating early surgical resection had better overall survival than those treated at a hospital advocating "watchful waiting," according to a report published online Oct. 30 in JAMA.

This finding significantly strengthens the sparse evidence in support of early resection for newly diagnosed diffuse low-grade gliomas, said Dr. Asgeir S. Jakola of the department of neurosurgery, St. Olav’s University Hospital, Trondheim (Norway) and his associates.

Management of these tumors is one of the major controversies in both neurology and oncology today, largely because the effect of surgery on survival is still unclear. The only evidence available until now was based solely on uncontrolled surgical series; some of these have reported that it is safe to withhold surgery until the lesions progress, while others have reported that immediate resection improves survival and delays the time to malignant transformation.

Both patients and physicians are reluctant to undertake immediate surgery when the evidence supporting that strategy has been so tenuous. They also are concerned that the risk of early and aggressive surgery outweighs the benefit, particularly when most patients are capable of normal activity and have a reasonably long life expectancy at diagnosis, the investigators said.

It is unlikely that a randomized, controlled study comparing the two approaches will ever be performed. Dr. Jakola and his colleagues therefore conducted a retrospective, population-based parallel-cohort study at two neurosurgical centers, each of which preferred one of these strategies over the other. Their "natural experiment" was possible because in Norway, there were two such facilities that were relatively close geographically and served a homogenous population. The nationalized health care system distributes training, resources, and personnel equally throughout the country, so the two hospitals were quite similar in other respects. And patient follow-up is 100%.

The 12-year study involved 153 adults with diffuse, histologically verified supratentorial grade I and II tumors diagnosed in 1998-2009, who were followed until death or until April 2011. The median follow-up was 7 years. Gliomas included astrocytomas, oligodendrogliomas, and oligoastrocytomas.

For patients with newly diagnosed low-grade gliomas, hospital A favored biopsy and watchful waiting. The 66 patients treated there typically were followed with MRI at 3 and 6 months, then yearly thereafter. They usually were offered surgical resection, if the lesions grew or showed signs of malignant transformation.

Hospital B favored immediate maximal safe tumor resection for the 87 patients treated there, with MRI follow-up at 6 and 12 months, then annually thereafter. This strategy was not pursued in some patients, however: notably, those who were elderly or had comorbidities and were likely to die from another cause before malignant transformation would take place, and those who had very widespread tumor infiltration that made resection impractical.

The two study groups were well balanced with regard to patient age and comorbidities, and rates of surgical rescue therapy were the same. There also were no differences between the two groups in complications or acquired neurologic deficits.

At the end of the study period, 34 patients (52%) from hospital A had died, compared with only 28 patients (32%) from hospital B. Median survival was 5.9 years at hospital A, but median survival had not yet been reached at hospital B, the researchers said (JAMA 2012;308: [doi:10.1001/jama.2012.12807]).

This survival advantage increased over time. Expected 3-year survival was 70% at hospital A vs. 80% at hospital B; expected 5-year survival was 60% at hospital A vs. 74% at hospital B; and expected 7-year survival was 44% at hospital A vs. 68% at hospital B.

In a post hoc analysis that attempted to account for differences between the two study groups in prognostic factors, the survival benefit for immediate resection remained robust. It also remained robust in another post hoc analysis that examined the subgroup of patients who had the most common glioma, a grade II astrocytoma. Median survival was 5.6 years at the hospital favoring watchful waiting, compared with 9.7 years at the hospital favoring early resection, in this large subgroup of patients.

Based on these findings, hospital A has changed its preferred strategy from watchful waiting to early resection, Dr. Jakola and his associates said.

"Despite the clear survival advantage seen, clinical judgment is still necessary in individual patients with suspected low-grade glioma since results will depend on patient and disease characteristics together with surgical results in terms of resection grades and complication rates," they added.

One of Dr. Jakola’s associates reported holding stock in Sonowand, manufacturer of the 3-D ultrasound-based imaging system used in one of the study hospitals.

Adults in Norway with diffuse low-grade gliomas who were treated at a hospital advocating early surgical resection had better overall survival than those treated at a hospital advocating "watchful waiting," according to a report published online Oct. 30 in JAMA.

This finding significantly strengthens the sparse evidence in support of early resection for newly diagnosed diffuse low-grade gliomas, said Dr. Asgeir S. Jakola of the department of neurosurgery, St. Olav’s University Hospital, Trondheim (Norway) and his associates.

Management of these tumors is one of the major controversies in both neurology and oncology today, largely because the effect of surgery on survival is still unclear. The only evidence available until now was based solely on uncontrolled surgical series; some of these have reported that it is safe to withhold surgery until the lesions progress, while others have reported that immediate resection improves survival and delays the time to malignant transformation.

Both patients and physicians are reluctant to undertake immediate surgery when the evidence supporting that strategy has been so tenuous. They also are concerned that the risk of early and aggressive surgery outweighs the benefit, particularly when most patients are capable of normal activity and have a reasonably long life expectancy at diagnosis, the investigators said.

It is unlikely that a randomized, controlled study comparing the two approaches will ever be performed. Dr. Jakola and his colleagues therefore conducted a retrospective, population-based parallel-cohort study at two neurosurgical centers, each of which preferred one of these strategies over the other. Their "natural experiment" was possible because in Norway, there were two such facilities that were relatively close geographically and served a homogenous population. The nationalized health care system distributes training, resources, and personnel equally throughout the country, so the two hospitals were quite similar in other respects. And patient follow-up is 100%.

The 12-year study involved 153 adults with diffuse, histologically verified supratentorial grade I and II tumors diagnosed in 1998-2009, who were followed until death or until April 2011. The median follow-up was 7 years. Gliomas included astrocytomas, oligodendrogliomas, and oligoastrocytomas.

For patients with newly diagnosed low-grade gliomas, hospital A favored biopsy and watchful waiting. The 66 patients treated there typically were followed with MRI at 3 and 6 months, then yearly thereafter. They usually were offered surgical resection, if the lesions grew or showed signs of malignant transformation.

Hospital B favored immediate maximal safe tumor resection for the 87 patients treated there, with MRI follow-up at 6 and 12 months, then annually thereafter. This strategy was not pursued in some patients, however: notably, those who were elderly or had comorbidities and were likely to die from another cause before malignant transformation would take place, and those who had very widespread tumor infiltration that made resection impractical.

The two study groups were well balanced with regard to patient age and comorbidities, and rates of surgical rescue therapy were the same. There also were no differences between the two groups in complications or acquired neurologic deficits.

At the end of the study period, 34 patients (52%) from hospital A had died, compared with only 28 patients (32%) from hospital B. Median survival was 5.9 years at hospital A, but median survival had not yet been reached at hospital B, the researchers said (JAMA 2012;308: [doi:10.1001/jama.2012.12807]).

This survival advantage increased over time. Expected 3-year survival was 70% at hospital A vs. 80% at hospital B; expected 5-year survival was 60% at hospital A vs. 74% at hospital B; and expected 7-year survival was 44% at hospital A vs. 68% at hospital B.

In a post hoc analysis that attempted to account for differences between the two study groups in prognostic factors, the survival benefit for immediate resection remained robust. It also remained robust in another post hoc analysis that examined the subgroup of patients who had the most common glioma, a grade II astrocytoma. Median survival was 5.6 years at the hospital favoring watchful waiting, compared with 9.7 years at the hospital favoring early resection, in this large subgroup of patients.

Based on these findings, hospital A has changed its preferred strategy from watchful waiting to early resection, Dr. Jakola and his associates said.

"Despite the clear survival advantage seen, clinical judgment is still necessary in individual patients with suspected low-grade glioma since results will depend on patient and disease characteristics together with surgical results in terms of resection grades and complication rates," they added.

One of Dr. Jakola’s associates reported holding stock in Sonowand, manufacturer of the 3-D ultrasound-based imaging system used in one of the study hospitals.

BOSTON – Memantine, a drug normally prescribed for slowing cognitive decline in Alzheimer’s disease, can help to preserve cognitive function in cancer patients who have undergone whole brain irradiation, a study showed.

In a phase III trial, patients with brain metastases were randomly assigned to take 20 mg memantine (Namenda) or placebo daily for 24 weeks after whole brain radiation therapy (WBRT). The memantine cohort had a 17% relative reduction in cognitive decline compared with patients who got a placebo, Dr. Nadia N. Laack reported at the annual meeting of the American Society for Radiation Oncology.

Courtesy of ASTRO

The finding teetered on the edge of statistical significance (P = .059), however, because only one-third of patients (32%) completed the 24 weeks of drug therapy, due to death (survival was poorer than expected), disease progression, or noncompliance, said Dr. Laack. a radiation oncologist at the Mayo Clinic in Rochester, Minn.

"Overall, we feel that the weight of evidence supports our conclusion that memantine helps to preserve cognitive function after whole brain radiotherapy in patients with brain metastases," Dr. Laack said at a briefing prior to presenting the data at a plenary session.

WBRT is associated with cognitive impairment in a majority of patients who receive it, Dr. Laack said, noting that at 4 months post radiation, 60% of patients will have declines in one or more cognitive domains.

Because the mechanism of decline is similar to that seen with Alzheimer\'s and vascular dementias, and because memantine has been shown to modestly improve mild to moderate cognition in both dementia types, Dr. Laack and his colleagues hypothesized that it might protect brains exposed to therapeutic doses of radiation.

A total of 508 patients were tested at baseline and at 8, 16, 24, and 52 weeks after radiation with 37.5 Gy in 15 fractions. They were evaluated with MRI and cognitive assessment; domains of memory, processing speed, executive function, global function, self-reported cognitive function, and quality of life were evaluated. Median overall follow-up was 12.4 months.

There were no differences between the treatment groups in overall survival at a median of 6 months or in progression-free survival at 5 months.

Among 149 patients available for analysis at 24 weeks, patients who took memantine had a significantly longer time to memory decline than did those on placebo (P = .02), and had a trend toward less decline in the primary end point, the Hopkins Verbal Learning Test–Revised delayed recall instrument (median decline of 0 standard deviation, vs. –2 standard deviations for patients on placebo).

For the secondary objective of cognitive function decline/failure, defined as a change greater than reversible cognitive impairment or 2 standard deviations decline from baseline on any domain of brain function, the hazard ratio for memantine at 24 weeks was 0.784 (P = .01), indicating a significant reduction in the incidence of cognitive dysfunction.

"Although memantine was discontinued at 6 months, the effect on cognitive function was maintained for the duration of the trial, suggesting that memantine may be preventing radiation injury rather than simply treating cognitive dysfunction," Dr. Laack said.

The trial was sponsored by grants from the National Cancer Institute and Forest Pharmaceuticals. Dr. Laack reported no relevant financial disclosures.

BOSTON – Memantine, a drug normally prescribed for slowing cognitive decline in Alzheimer’s disease, can help to preserve cognitive function in cancer patients who have undergone whole brain irradiation, a study showed.

In a phase III trial, patients with brain metastases were randomly assigned to take 20 mg memantine (Namenda) or placebo daily for 24 weeks after whole brain radiation therapy (WBRT). The memantine cohort had a 17% relative reduction in cognitive decline compared with patients who got a placebo, Dr. Nadia N. Laack reported at the annual meeting of the American Society for Radiation Oncology.

Courtesy of ASTRO

The finding teetered on the edge of statistical significance (P = .059), however, because only one-third of patients (32%) completed the 24 weeks of drug therapy, due to death (survival was poorer than expected), disease progression, or noncompliance, said Dr. Laack. a radiation oncologist at the Mayo Clinic in Rochester, Minn.

"Overall, we feel that the weight of evidence supports our conclusion that memantine helps to preserve cognitive function after whole brain radiotherapy in patients with brain metastases," Dr. Laack said at a briefing prior to presenting the data at a plenary session.

WBRT is associated with cognitive impairment in a majority of patients who receive it, Dr. Laack said, noting that at 4 months post radiation, 60% of patients will have declines in one or more cognitive domains.

Because the mechanism of decline is similar to that seen with Alzheimer\'s and vascular dementias, and because memantine has been shown to modestly improve mild to moderate cognition in both dementia types, Dr. Laack and his colleagues hypothesized that it might protect brains exposed to therapeutic doses of radiation.

A total of 508 patients were tested at baseline and at 8, 16, 24, and 52 weeks after radiation with 37.5 Gy in 15 fractions. They were evaluated with MRI and cognitive assessment; domains of memory, processing speed, executive function, global function, self-reported cognitive function, and quality of life were evaluated. Median overall follow-up was 12.4 months.

There were no differences between the treatment groups in overall survival at a median of 6 months or in progression-free survival at 5 months.

Among 149 patients available for analysis at 24 weeks, patients who took memantine had a significantly longer time to memory decline than did those on placebo (P = .02), and had a trend toward less decline in the primary end point, the Hopkins Verbal Learning Test–Revised delayed recall instrument (median decline of 0 standard deviation, vs. –2 standard deviations for patients on placebo).

For the secondary objective of cognitive function decline/failure, defined as a change greater than reversible cognitive impairment or 2 standard deviations decline from baseline on any domain of brain function, the hazard ratio for memantine at 24 weeks was 0.784 (P = .01), indicating a significant reduction in the incidence of cognitive dysfunction.

"Although memantine was discontinued at 6 months, the effect on cognitive function was maintained for the duration of the trial, suggesting that memantine may be preventing radiation injury rather than simply treating cognitive dysfunction," Dr. Laack said.

The trial was sponsored by grants from the National Cancer Institute and Forest Pharmaceuticals. Dr. Laack reported no relevant financial disclosures.

BOSTON – Memantine, a drug normally prescribed for slowing cognitive decline in Alzheimer’s disease, can help to preserve cognitive function in cancer patients who have undergone whole brain irradiation, a study showed.

In a phase III trial, patients with brain metastases were randomly assigned to take 20 mg memantine (Namenda) or placebo daily for 24 weeks after whole brain radiation therapy (WBRT). The memantine cohort had a 17% relative reduction in cognitive decline compared with patients who got a placebo, Dr. Nadia N. Laack reported at the annual meeting of the American Society for Radiation Oncology.

Courtesy of ASTRO

The finding teetered on the edge of statistical significance (P = .059), however, because only one-third of patients (32%) completed the 24 weeks of drug therapy, due to death (survival was poorer than expected), disease progression, or noncompliance, said Dr. Laack. a radiation oncologist at the Mayo Clinic in Rochester, Minn.

"Overall, we feel that the weight of evidence supports our conclusion that memantine helps to preserve cognitive function after whole brain radiotherapy in patients with brain metastases," Dr. Laack said at a briefing prior to presenting the data at a plenary session.

WBRT is associated with cognitive impairment in a majority of patients who receive it, Dr. Laack said, noting that at 4 months post radiation, 60% of patients will have declines in one or more cognitive domains.

Because the mechanism of decline is similar to that seen with Alzheimer\'s and vascular dementias, and because memantine has been shown to modestly improve mild to moderate cognition in both dementia types, Dr. Laack and his colleagues hypothesized that it might protect brains exposed to therapeutic doses of radiation.

A total of 508 patients were tested at baseline and at 8, 16, 24, and 52 weeks after radiation with 37.5 Gy in 15 fractions. They were evaluated with MRI and cognitive assessment; domains of memory, processing speed, executive function, global function, self-reported cognitive function, and quality of life were evaluated. Median overall follow-up was 12.4 months.

There were no differences between the treatment groups in overall survival at a median of 6 months or in progression-free survival at 5 months.

Among 149 patients available for analysis at 24 weeks, patients who took memantine had a significantly longer time to memory decline than did those on placebo (P = .02), and had a trend toward less decline in the primary end point, the Hopkins Verbal Learning Test–Revised delayed recall instrument (median decline of 0 standard deviation, vs. –2 standard deviations for patients on placebo).

For the secondary objective of cognitive function decline/failure, defined as a change greater than reversible cognitive impairment or 2 standard deviations decline from baseline on any domain of brain function, the hazard ratio for memantine at 24 weeks was 0.784 (P = .01), indicating a significant reduction in the incidence of cognitive dysfunction.

"Although memantine was discontinued at 6 months, the effect on cognitive function was maintained for the duration of the trial, suggesting that memantine may be preventing radiation injury rather than simply treating cognitive dysfunction," Dr. Laack said.

The trial was sponsored by grants from the National Cancer Institute and Forest Pharmaceuticals. Dr. Laack reported no relevant financial disclosures.

Patients with a life-limiting illness frequently experience pain and other symptoms. It is important to pay close attention when medication therapy is used to manage these symptoms. Occasionally, practitioners need to be creative in selecting, dosing, administering, and discontinuing medications at the end of life because of the patient’s changing health care needs.

In the video below, Dr. Kathryn Walker and Dr. Lynn McPherson of the University of Maryland discuss the role of the pharmacist in the hospital and hospice settings, as well as a few of their favorite medication tips and tricks in end-of-life care.

This article offers practical end-of-life medication tips including, but not limited to, medication administration; guidance on how to increase and decrease doses; medication selection for difficult to-treat patients; alternative dosage formulations; routes of medication administration; debridement medication regimens; and appropriate drug therapy selection. Dr. McPherson and Dr. Walker discuss how to deal with changing the goals of care  for your dying patients and their families. They offer suggestions on how to integrate some helpful end-of-life medication tips into your practice.

*For a PDF of the full article, click on the link to the left of this introduction.

Patients with a life-limiting illness frequently experience pain and other symptoms. It is important to pay close attention when medication therapy is used to manage these symptoms. Occasionally, practitioners need to be creative in selecting, dosing, administering, and discontinuing medications at the end of life because of the patient’s changing health care needs.

In the video below, Dr. Kathryn Walker and Dr. Lynn McPherson of the University of Maryland discuss the role of the pharmacist in the hospital and hospice settings, as well as a few of their favorite medication tips and tricks in end-of-life care.

This article offers practical end-of-life medication tips including, but not limited to, medication administration; guidance on how to increase and decrease doses; medication selection for difficult to-treat patients; alternative dosage formulations; routes of medication administration; debridement medication regimens; and appropriate drug therapy selection. Dr. McPherson and Dr. Walker discuss how to deal with changing the goals of care  for your dying patients and their families. They offer suggestions on how to integrate some helpful end-of-life medication tips into your practice.

*For a PDF of the full article, click on the link to the left of this introduction.

Patients with a life-limiting illness frequently experience pain and other symptoms. It is important to pay close attention when medication therapy is used to manage these symptoms. Occasionally, practitioners need to be creative in selecting, dosing, administering, and discontinuing medications at the end of life because of the patient’s changing health care needs.

In the video below, Dr. Kathryn Walker and Dr. Lynn McPherson of the University of Maryland discuss the role of the pharmacist in the hospital and hospice settings, as well as a few of their favorite medication tips and tricks in end-of-life care.

This article offers practical end-of-life medication tips including, but not limited to, medication administration; guidance on how to increase and decrease doses; medication selection for difficult to-treat patients; alternative dosage formulations; routes of medication administration; debridement medication regimens; and appropriate drug therapy selection. Dr. McPherson and Dr. Walker discuss how to deal with changing the goals of care  for your dying patients and their families. They offer suggestions on how to integrate some helpful end-of-life medication tips into your practice.

*For a PDF of the full article, click on the link to the left of this introduction.

CHICAGO – Outcomes for children seen at pediatric trauma centers were not significantly different than for children seen at adult trauma centers, according to a review of more than 45,000 pediatric injuries.

The finding "has significant policy implications because it means that emergency medical services do not have to triage patients according to specialty care centers," and it informs discussions about pediatric access to trauma care, said researcher Dr. Cassandra Villegas of the University of Arizona in Tucson.

Trauma accounts for approximately one-third of all pediatric mortality, but there are only 170 pediatric-specific trauma centers in the United States, which "means that the vast majority of pediatric patients that are injured are actually managed and evaluated at adult trauma centers," Dr. Villegas said at the annual clinical congress of the American College of Surgeons.

Nonetheless, data on pediatric outcomes for children treated at pediatric vs. adult trauma centers have not been conclusive, and most previous studies have focused on metropolitan or state pediatric centers, she said.

Dr. Villegas and her colleagues reviewed data from the National Trauma Database for 2007-2008 that included 27 pediatric trauma centers and 30 adult (mixed care) centers that had pediatric beds. Most (90%) of the 30 mixed care centers provided all acute pediatric services, while 10% shared these services with another medical center. All of the pediatric centers and 90% of the mixed care centers had pediatric intensive care units. The pediatric centers were significantly more likely to be university hospitals than were the mixed centers (85% vs. 53%).

The researchers analyzed outcomes for children aged 0-14 years, including 33,327 patients treated at pediatric centers and 12,605 patients treated at mixed centers.

After controlling for multiple variables including injury characteristics, Dr. Villegas and her associates found that in-hospital mortality – the primary outcome – was twice as high at mixed centers as at pediatric centers (2% vs. 1%), but this difference was not significant. The median length of stay was 2 days at all centers, although ICU admission rates were higher at mixed centers vs. pediatric centers (26% vs. 14%).

Approximately one-third of the patients seen at either type of center had an Injury Severity Score (ISS) in the 9-15 range, said Dr. Villegas. Falls were the most common type of injury, accounting for 49% of cases at pediatric centers and 37% of cases at mixed centers.

The patients at mixed centers were more likely than those at pediatric centers to be hypotensive (18% vs. 10%).

The study was limited by several factors, including the low incidence of pediatric mortality, the lack of uniform coding for death on arrival, and differences in ICU admission practices, said Dr. Villegas.

However, the findings suggest that there are no differences in outcomes for children treated at pediatric vs. mixed care centers, she said.

Dr. Villegas reported having no financial conflicts of interest.

CHICAGO – Outcomes for children seen at pediatric trauma centers were not significantly different than for children seen at adult trauma centers, according to a review of more than 45,000 pediatric injuries.

The finding "has significant policy implications because it means that emergency medical services do not have to triage patients according to specialty care centers," and it informs discussions about pediatric access to trauma care, said researcher Dr. Cassandra Villegas of the University of Arizona in Tucson.

Trauma accounts for approximately one-third of all pediatric mortality, but there are only 170 pediatric-specific trauma centers in the United States, which "means that the vast majority of pediatric patients that are injured are actually managed and evaluated at adult trauma centers," Dr. Villegas said at the annual clinical congress of the American College of Surgeons.

Nonetheless, data on pediatric outcomes for children treated at pediatric vs. adult trauma centers have not been conclusive, and most previous studies have focused on metropolitan or state pediatric centers, she said.

Dr. Villegas and her colleagues reviewed data from the National Trauma Database for 2007-2008 that included 27 pediatric trauma centers and 30 adult (mixed care) centers that had pediatric beds. Most (90%) of the 30 mixed care centers provided all acute pediatric services, while 10% shared these services with another medical center. All of the pediatric centers and 90% of the mixed care centers had pediatric intensive care units. The pediatric centers were significantly more likely to be university hospitals than were the mixed centers (85% vs. 53%).

The researchers analyzed outcomes for children aged 0-14 years, including 33,327 patients treated at pediatric centers and 12,605 patients treated at mixed centers.

After controlling for multiple variables including injury characteristics, Dr. Villegas and her associates found that in-hospital mortality – the primary outcome – was twice as high at mixed centers as at pediatric centers (2% vs. 1%), but this difference was not significant. The median length of stay was 2 days at all centers, although ICU admission rates were higher at mixed centers vs. pediatric centers (26% vs. 14%).

Approximately one-third of the patients seen at either type of center had an Injury Severity Score (ISS) in the 9-15 range, said Dr. Villegas. Falls were the most common type of injury, accounting for 49% of cases at pediatric centers and 37% of cases at mixed centers.

The patients at mixed centers were more likely than those at pediatric centers to be hypotensive (18% vs. 10%).

The study was limited by several factors, including the low incidence of pediatric mortality, the lack of uniform coding for death on arrival, and differences in ICU admission practices, said Dr. Villegas.

However, the findings suggest that there are no differences in outcomes for children treated at pediatric vs. mixed care centers, she said.

Dr. Villegas reported having no financial conflicts of interest.

CHICAGO – Outcomes for children seen at pediatric trauma centers were not significantly different than for children seen at adult trauma centers, according to a review of more than 45,000 pediatric injuries.

The finding "has significant policy implications because it means that emergency medical services do not have to triage patients according to specialty care centers," and it informs discussions about pediatric access to trauma care, said researcher Dr. Cassandra Villegas of the University of Arizona in Tucson.

Trauma accounts for approximately one-third of all pediatric mortality, but there are only 170 pediatric-specific trauma centers in the United States, which "means that the vast majority of pediatric patients that are injured are actually managed and evaluated at adult trauma centers," Dr. Villegas said at the annual clinical congress of the American College of Surgeons.

Nonetheless, data on pediatric outcomes for children treated at pediatric vs. adult trauma centers have not been conclusive, and most previous studies have focused on metropolitan or state pediatric centers, she said.

Dr. Villegas and her colleagues reviewed data from the National Trauma Database for 2007-2008 that included 27 pediatric trauma centers and 30 adult (mixed care) centers that had pediatric beds. Most (90%) of the 30 mixed care centers provided all acute pediatric services, while 10% shared these services with another medical center. All of the pediatric centers and 90% of the mixed care centers had pediatric intensive care units. The pediatric centers were significantly more likely to be university hospitals than were the mixed centers (85% vs. 53%).

The researchers analyzed outcomes for children aged 0-14 years, including 33,327 patients treated at pediatric centers and 12,605 patients treated at mixed centers.

After controlling for multiple variables including injury characteristics, Dr. Villegas and her associates found that in-hospital mortality – the primary outcome – was twice as high at mixed centers as at pediatric centers (2% vs. 1%), but this difference was not significant. The median length of stay was 2 days at all centers, although ICU admission rates were higher at mixed centers vs. pediatric centers (26% vs. 14%).

Approximately one-third of the patients seen at either type of center had an Injury Severity Score (ISS) in the 9-15 range, said Dr. Villegas. Falls were the most common type of injury, accounting for 49% of cases at pediatric centers and 37% of cases at mixed centers.

The patients at mixed centers were more likely than those at pediatric centers to be hypotensive (18% vs. 10%).

The study was limited by several factors, including the low incidence of pediatric mortality, the lack of uniform coding for death on arrival, and differences in ICU admission practices, said Dr. Villegas.

However, the findings suggest that there are no differences in outcomes for children treated at pediatric vs. mixed care centers, she said.

Dr. Villegas reported having no financial conflicts of interest.