The functional effects of head injury in the elderly

Wilson, Janet A.; Pentland, Brian T.; Currie, CJ; Miller, Jay D.

doi:10.3109/02699058709034456

Cited by 29 publications

(11 citation statements)

References 9 publications

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“…This has been a subject of several prior studies and it has become well established that falls predominate as a cause of head injury in the elderly whereas road accidents are more often responsible in the young (Amacher and Bybee, 1987;Diamond, 1996;Mosenthal et al, 2002;Strang et al, 1978;Wilson et al, 1987). The inversion of mechanism preponderance is observed in the age of 60 (Diamond, 1996), and our data confirm this.…”

Section: Figsupporting

confidence: 86%

Head Injury Mortality in a Geriatric Population: Differentiating an “Edge” Age Group with Better Potential for Benefit than Older Poor-Prognosis Patients

Bouras

Stranjalis

Korfias

et al. 2007

Journal of Neurotrauma

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A comparison of outcomes between different modes of head-injury treatment in the elderly has important bearing on questions of cost-effectiveness and medical ethics. Here, we have examined rates of mortality in elderly head-trauma victims to determine whether it is valid to differentiate an "edge" age group of younger elderly patients, 65-74 years of age, from older elderly patients, considering possible benefit from intensive treatment and surgical intervention. We collected data from 1926 cases of head trauma and separated them into three age groups: 14-64 years, 65-74 years, and 75 years or older. We then compared these groups with respect to cause of injury, severity of injury, and whether or not treatment included either admission to an Intensive Care Unit (ICU) or surgical intervention. We found that road traffic accidents were the major cause of head injury in the younger age group, whereas in the elderly falls predominated. Mortality was higher in the elderly in all the head injury severity subgroups. Young subjects with a Glasgow Coma Scale (GCS) score of less than or equal to 8 tended to benefit from ICU treatment whereas patients 75 and over did not, regardless of their severity of injury. For these patients who were in the 65-74 age group, the data suggested that some benefit was likely. Patients 75 and older were significantly less likely to survive surgical intervention than younger patients. We conclude that it is valid to treat patients in the age group 65-74 years as a separate group from those patients 75 and older. Patients in this younger subset of the elderly may benefit from ICU treatment or surgical intervention. However, the patients in our older subset of elderly patients clearly did not, and they had a significantly higher risk of surgical mortality.

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Section: Figsupporting

confidence: 86%

Head Injury Mortality in a Geriatric Population: Differentiating an “Edge” Age Group with Better Potential for Benefit than Older Poor-Prognosis Patients

Bouras

Stranjalis

Korfias

et al. 2007

Journal of Neurotrauma

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“…'429 Caution must be exercised, however, in concluding that older adults necessarily have a poor outcome. As 19 of the 22 patients were tested within three months of injury, our findings characterise the initial stage of recovery and do not address long term functioning. It is conceivable that a number of patients will exhibit improvement.…”

Section: Discussionmentioning

confidence: 79%

“…In contrast, the proportion of perseverative errors, such as repeating earlier items or varying them only slightly (for example, "find" and "finding"), did not significantly differ between the groups (patients: mean = 0 04, SD 0O07; controls: mean = 0 05, SD 0-05). [16][17][18][19][20]. Figure 1 displays the mean percentage of words recalled on each trial of the CVLT for patients and controls.…”

Section: Methodsmentioning

confidence: 99%

Neurobehavioural consequences of closed head injury in older adults.

Goldstein

Levin

Presley

et al. 1994

Journal of Neurology, Neurosurgery & Psychiatry

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This study examined the neurobehavioural effects of closed head injury (CHI) in adults aged 50 years and older. Twenty two mild to moderate CHI patients who were within seven months of the injury were administered measures of language, memory, attention, and executive functioning. Compared with demographically similar normal controls, the patients exhibited significandy poorer functioning on the cognitive domains. Naming and word fluency under timed conditions, verbal and visual memory, and the ability to infer similarities were especially vulnerable. These initial findings indicate that CHI in older adults produces considerable cognitive deficits in the early stages of recovery. Future research should characterise long term outcome and the potential links between head injury and the development of progressive dementia. Apart from these studies of global outcome, little is known about cognitive functioning in older CHI patients. An exception is a recent study'0 which examined cognitive performance in patients who were 50-75 years old at the time of their injuries. Seventy patients were administered tests of general intellectual functioning, memory, language, and visuomotor abilities. Mazzucchi and colleagues'0 found that 50% of their patients exhibited generalised deterioration and dementia, whereas only 25% had minimal or no deterioration. Moreover, patients with mild head injuries, ie, no loss of consciousness, Glasgow coma scale" scores of 13-15, post-traumatic amnesia of <1 day, and normal CT head scans were no more likely to have a better outcome than those with severe injuries. Generalised deterioration and dementia were common in both groups with mild and moderate to severe injury. The study of Mazzucchi et al'0 represents an important first step in describing neurobehavioural functioning in the older head injured population. Their research indicates that CHI produces cognitive deficits across the injury severity spectrum. However, one limitation is that Mazzucchi et al did not examine specific cognitive features, such as memory and language. Instead, they made a gross classification of groups according to impairment on any of these measures. Moreover, their patients were tested from six months to three years after injury. Therefore, early neurobehavioural performance was not characterised.The present study provided an initial examination of the early neurobehavioural features of individuals who were > 50 years and sustained mild to moderate head injuries. We evaluated abilities which are frequently compromised after CHI in young adults, including expressive language,'2 memory,'3 14 attention,'5 and executive processing.'6 We also compared pre-and postinjury living and employment status in a subset of patients. Methods SUBJECTSProspective data were collected on 18 men and four women aged ) 50 years who sustained mild to moderate CHI. Patients were recruited from acute care hospitals affiliated with the Emory University School of Medicine in Atlanta and the University of Texas Medical Schools in Ga...

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“…This is reflected in the fact that the highest rates of TBI-associated hospitalizations and death occur in the elderly even though the elderly are ranked as the third highest age group for TBI incidence (Susman et al, 2002, Stocchetti et al, 2012). Aged adults are more likely to remain severely disabled or vegetative after TBI as compared to young adults, and 91% of severe TBI patients older than 56 years suffer significant disability (Wilson et al, 1988, Stocchetti et al, 2012). Even a mild TBI that produces only a temporary cognitive impairment in a young adult can result in a significant, prolonged cognitive disability in an aged adult (Susman et al, 2002).…”

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confidence: 99%

Age-dependent alterations in cAMP signaling contribute to synaptic plasticity deficits following traumatic brain injury

et al. 2013

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The elderly have comparatively worse cognitive impairments from traumatic brain injury (TBI) relative to younger adults, but the molecular mechanisms that underlie this exacerbation of cognitive deficits are unknown. Experimental models of TBI have demonstrated that the cyclic AMP-protein kinase A (cAMP-PKA) signaling pathway is downregulated after brain trauma. Since the cAMPPKA signaling pathway is a key mediator of long-term memory formation, we investigated whether the TBI-induced decrease in cAMP levels is exacerbated in aged animals. Aged (19 months) and young adult (3 months) male Fischer 344 rats received sham surgery or mild (1.4–1.6 atmospheres, atm) or moderate (1.7–2.1 atm) parasagittal fluid-percussion brain injury. At various time points after surgery, the ipsilateral parietal cortex, hippocampus, and thalamus were assayed for cAMP levels. Mild TBI lowered cAMP levels in the hippocampus of aged, but not young adult animals. Moderate TBI lowered cAMP levels in the hippocampus and parietal cortex of both age groups. In the thalamus, cAMP levels were significantly lowered after moderate, but not mild TBI. To determine if the TBI-induced decreases in cAMP had physiological consequences in aged animals, hippocampal long-term potentiation (LTP) in the Schaffer collateral pathway of the CA1 region was assessed. LTP was significantly decreased in both young adult and aged animals after mild and moderate TBI as compared to sham surgery animals. Rolipram rescued the LTP deficits after mild TBI for young adult animals and caused a partial recovery for aged animals. However, rolipram did not rescue LTP deficits after moderate TBI in either young adult or aged animals. These results indicate that exacerbation of cognitive impairments in aged animals with TBI may be due to decreased cAMP levels and deficits in hippocampal LTP.

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The functional effects of head injury in the elderly

Cited by 29 publications

References 9 publications

Head Injury Mortality in a Geriatric Population: Differentiating an “Edge” Age Group with Better Potential for Benefit than Older Poor-Prognosis Patients

Head Injury Mortality in a Geriatric Population: Differentiating an “Edge” Age Group with Better Potential for Benefit than Older Poor-Prognosis Patients

Neurobehavioural consequences of closed head injury in older adults.

Age-dependent alterations in cAMP signaling contribute to synaptic plasticity deficits following traumatic brain injury

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