Cerebrocerebellar hypometabolism associated with repetitive blast exposure mild traumatic brain injury in 12 Iraq war Veterans with persistent post-concussive symptoms

Authors: Elaine R. Peskind a c, Eric C. Petrie a c, Donna J. Cross d, Kathleen Pagulayan ac, Kathleen McCraw a, David Hoffa, Kim Hart a, Chang-En Yu b, e, Murray A. Raskind a, c, David G. Cook b, e and Satoshi Minoshima d

Disagreement exists regarding the extent to which persistent post-concussive symptoms (PCS) reported by Iraq combat Veterans with repeated episodes of mild traumatic brain injury (mTBI) from explosive blasts represent structural or functional brain damage or an epiphenomenon of comorbid depression or posttraumatic stress disorder (PTSD). Objective assessment of brain function in this population may clarify the issue. To this end, twelve Iraq war Veterans (32.0 ± 8.5 years of age) reporting one or more blast exposures meeting American Congress of Rehabilitation Medicine criteria for mTBI and persistent PCS and 12 cognitively normal community volunteers (53.0 ± 4.6 years of age) without history of head trauma underwent brain fluorodeoxyglucose positron emission tomography (FDG-PET) and neuropsychological assessments and completed PCS and psychiatric symptom rating scales. Compared to controls, Veterans with mTBI (with or without PTSD) exhibited decreased cerebral metabolic rate of glucose in the cerebellum, vermis, pons, and medial temporal lobe. They also exhibited subtle impairments in verbal fluency, cognitive processing speed, attention, and working memory, similar to those reported in the literature for patients with cerebellar lesions. These FDG-PET imaging findings suggest that regional brain hypometabolism may constitute a neurobiological substrate for chronic PCS in Iraq combat Veterans with repetitive blast-trauma mTBI. Given the potential public health implications of these findings, further investigation of brain function in these Veterans appears warranted.

Intracranial pressure monitoring

Authors: R. Ravi a and R. J. Morgan b

Maintaining adequate cerebral perfusion is the primary goal of management of patients with traumatic brain injury and intracranial pressure is one of the major factors affecting cerebral blood flow. Intracranial pressure measurement is necessary to confirm or exclude intracranial hypertension and to determine cerebral perfusion pressure. It also helps guide therapy in head injury patients. There is a substantial body of evidence to support the use of intracranial pressure monitoring and it is now a central part of the critical care management of the severely brain injured patient. This is a review of intracranial pressure monitoring with specific reference to traumatic brain injury. A brief description of the physiology of cerebral blood flow and intracranial pressure is given followed by the principles of measurement, indications, techniques and problems associated with intracranial pressure monitoring.

Alzheimer's disease-related changes in diseases characterized by elevation of intracranial or intraocular pressure

Authors: Peter Wostyn a, Kurt Audenaert b and Peter Paul De Deyn c, d

In this review, we focus on the coexistence of Alzheimer's disease-related changes in brain diseases, such as normal pressure hydrocephalus and traumatic brain injury, and in glaucoma at the level of the retinal ganglion cells. This is a group of diseases that affect central nervous system tissue and are characterized by elevation of intracranial or intraocular pressure and/or local shear stress and strain. In considering possible mechanisms underlying Alzheimer-type changes in these diseases, we briefly summarize recent evidence indicating that caspase activation and abnormal processing of β-amyloid precursor protein, which are important events in Alzheimer's disease, may play a role both in glaucoma and following traumatic brain injury. With regard to normal pressure hydrocephalus, evidence suggests that changes in cerebrospinal fluid circulatory dynamics ultimately may result in reduced clearance of neurotoxins, such as β-amyloid peptides and tau protein, that play a role in the pathogenesis of Alzheimer's disease. Data presented in this review could be interpreted to suggest that Alzheimer-type changes in these diseases may result at least in part from exposure of central nervous system tissue to increased levels of mechanical stress. Evidence for such a relationship is of major importance because it may support an association between elevated mechanical load and the development of Alzheimer-type lesions. Further studies are warranted, however, especially to elucidate the role of elevated mechanical forces in Alzheimer's disease neuropathogenesis.

Bomb blast, mild traumatic brain injury and psychiatric morbidity: A review

Authors: Jeffrey V. Rosenfeld a, b and Nick L. Ford c

Traumatic brain injury (TBI) arising from blast exposure during war is common, and frequently complicated by psychiatric morbidity. There is controversy as to whether mild TBI from blast is different from other causes of mild TBI. Anxiety and affective disorders such as Post-traumatic Stress Disorder (PTSD) and depression are common accompaniments of blast injury with a significant overlap in the diagnostic features of PTSD with post-concussive syndrome (PCS). This review focuses on this overlap and the effects of mild TBI due to bomb blast. Mild TBI may have been over diagnosed by late retrospective review of returned servicemen and women using imprecise criteria. There is therefore a requirement for clear and careful documentation by health professionals of a TBI due to bomb blast shortly after the event so that the diagnosis of TBI can be made with confidence. There is a need for the early recognition of symptoms of PCS, PTSD and depression and early multi-disciplinary interventions focussed on expected return to duties. There also needs to be a continued emphasis on the de-stigmatisation of psychological conditions in military personnel returning from deployment.

Are intracranial pressure fluctuations important in glaucoma?

Authors: Peter Wostyna, Veva De Grootb, Kurt Audenaertc and Peter Paul De Deynd, e

Glaucoma is one of the leading causes of irreversible blindness. Primary open-angle glaucoma (POAG), the most common type, is a progressive optic neuropathy with characteristic structural changes in the optic nerve head and functional changes in the visual field. Mechanical and vascular theories for the pathogenesis of glaucomatous optic neuropathy have been proposed. Elevated intraocular pressure (IOP) is a strong risk factor, although a subset of POAG patients has normal IOP and is designated normal tension glaucoma (NTG). Clearly, factors other than IOP are likely to be involved in retinal ganglion cell death in glaucoma. An intriguing finding of recent studies is that intracranial pressure (ICP) is lower in patients with POAG and NTG when compared with nonglaucomatous control subjects. It has been suggested that the relationship between IOP and ICP may play a fundamental role in the development of glaucoma. A decreased ICP could result in an increased trans-lamina cribrosa pressure difference (IOP minus ICP) and lead to glaucomatous damage. In the present paper, we raise the question of whether ICP fluctuations also may be important in glaucoma. The effect of ICP fluctuation might be comparable to that of IOP fluctuation, which has been recognized as an independent risk factor for glaucoma progression.

Pulsatile Intracranial Pressure and Cerebral Autoregulation After Traumatic Brain Injury

Authors: Radolovich DK, Aries MJ, Castellani G, Corona A, Lavinio A, Smielewski P, Pickard JD, Czosnyka M.

BACKGROUND: Strong correlation between mean intracranial pressure (ICP) and its pulse wave amplitude (AMP) has been demonstrated in different clinical scenarios. We investigated the relationship between invasive mean arterial blood pressure (ABP) and AMP to explore its potential role as a descriptor of cerebrovascular pressure reactivity after traumatic brain injury (TBI).

METHODS: We retrospectively analyzed data of patients suffering from TBI with brain monitoring. Transcranial Doppler blood flow velocity, ABP, ICP were recorded digitally. Cerebral perfusion pressure (CPP) and AMP were derived. A new index-pressure-amplitude index (PAx)-was calculated as the Pearson correlation between (averaged over 10 s intervals) ABP and AMP with a 5 min long moving average window. The previously introduced transcranial Doppler-based autoregulation index Mx was evaluated in a similar way, as the moving correlation between blood flow velocity and CPP. The clinical outcome was assessed after 6 months using the Glasgow outcome score.

RESULTS: 293 patients were studied. The mean PAx was -0.09 (standard deviation 0.21). This negative value indicates that, on average, an increase in ABP causes a decrease in AMP and vice versa. PAx correlated strong with Mx (R (2) = 0.46, P < 0.0002). PAx also correlated with age (R (2) = 0.18, P < 0.05). PAx was found to have as good predictive outcome value (area under curve 0.71, P < 0.001) as Mx (area under curve 0.69, P < 0.001).

CONCLUSIONS: We demonstrated significant correlation between the known cerebral autoregulation index Mx and PAx. This new index of cerebrovascular pressure reactivity using ICP pulse wave information showed to have a strong association with outcome in TBI patients.


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