Severe Diffuse Brain Injury Research Articles

Autonomic Hyperactivity

Autonomic hyperactivity is a relatively common consequence of severe acute brain injury and can also be seen with spinal cord and peripheral nerve disorders. This article reviews basic pathophysiologic concepts regarding autonomic hyperactivity, its various forms of clinical presentation, and practical management considerations. Paroxysmal sympathetic hyperactivity is most common after traumatic brain injury but can also occur after other forms of severe acute diffuse or multifocal brain injury. Formal criteria for the diagnosis and severity grading of paroxysmal sympathetic hyperactivity have now been proposed. A growing body of literature is beginning to elucidate the mechanisms underlying this disorder, but treatment remains based on observational data. Our mechanistic understanding of other distinct forms of autonomic hyperactivity, such as autonomic dysreflexia after traumatic spinal cord injury and dysautonomia after Guillain-Barré syndrome, remains rudimentary, yet clinical experience shows that their appropriate management can minimize the risk of serious complications. Syndromes of autonomic hyperactivity can result from injury at all levels of the neuraxis. Much more research is needed to refine our understanding of these disorders and guide optimal management decisions.

Autoregulation of cerebral blood flow in severe diffuse axonal brain injury: the role of neuroanatomical factors

The study aim was to assess the effect of anatomical injuries to deep brain structures on the extent and duration of ACBF abnormalities in a model of severe diffuse axonal injury (DAI). The study demonstrated that brain injury in the projection of a dopaminergic structure (substantia nigra) and a cholinergic structure (nucleus basalis of Meynert region) was more common in patients with impaired ACBF and was associated with a longer duration of the impairment. The obtained data may indicate the presence of central (neurogenic) pathways of cerebral vessel tone regulation; traumatic injury of the pathways leads to a more severe and prolonged period of impaired ACBF. Probably, injury to these regulatory structures in some patients has an indirect effect on the course of intracranial hypertension. Further experimental and clinical studies in this direction are needed to elucidate all elements of neurogenic regulation of cerebral vessel tone and ACBF mechanisms.

Hypertension-Induced Enhanced Myogenic Constriction of Cerebral Arteries Is Preserved after Traumatic Brain Injury.

Traumatic brain injury (TBI) was shown to impair pressure-induced myogenic response of cerebral arteries, which is associated with vascular and neural dysfunction and increased mortality of TBI patients. Hypertension was shown to enhance myogenic tone of cerebral arteries via increased vascular production of 20-hydroxyeicosatrienoic acid (HETE). This adaptive mechanism protects brain tissue from pressure/volume overload; however, it can also lead to increased susceptibility to cerebral ischemia. Although both effects may potentiate the detrimental vascular consequences of TBI, it is not known how hypertension modulates the effect of TBI on myogenic responses of cerebral vessels. We hypothesized that in hypertensive rats, the enhanced myogenic cerebrovascular response is preserved after TBI. Therefore, we investigated the myogenic responses of isolated middle cerebral arteries (MCA) of normotensive and spontaneously hypertensive rats (SHR) after severe impact acceleration diffuse brain injury. TBI diminished myogenic constriction of MCAs isolated from normotensive rats, whereas the 20-HETE-mediated enhanced myogenic response of MCAs isolated from SHRs was not affected by TBI. These results suggest that the optimal cerebral perfusion pressure values and vascular signaling pathways can be different and, therefore, should be targeted differently in normotensive and hypertensive patients following TBI.

Enhanced myogenic response of cerebral arteries induced by pre‐existing hypertension is intact after traumatic brain injury

Traumatic brain injury (TBI) impairs pressure‐induced myogenic autoregulation of cerebral blood flow (CBF), which is associated with increased mortality and bad functional outcome of TBI patients. When blood pressure drops lack of myogenic autoregulatory function of cerebral vessels exposes brain tissue to hypoperfusion and ischemia; in case of high blood pressure it allows high blood volume to penetrate the brain exacerbating disruption of the blood brain barrier, development of hemorrhages and elevation of intracranial pressure. Hypertension, the most important cardiovascular risk factor in TBI patients, enhances myogenic tone of cerebral arteries via increased vascular production of 20‐hydroxyeicosatrienoic acid (HETE), which protects brain tissue form pressure/volume overload but leads to increased susceptibility to cerebral ischemia. Although both effects may potentiate the vascular consequences of TBI, it is not known how hypertension modulates the effect of TBI on myogenic responses of cerebral vessels. To establish the effect of TBI on cerebral myogenic responses in hypertension we studied isolated middle cerebral arteries (MCA) of normotensive and spontaneously hypertensive rats (SHR) after severe impact acceleration diffuse brain injury. We found that TBI diminished myogenic constriction of MCAs in normotensive animals, but the 20‐HETE mediated enhanced myogenic tone in SHRs was not affected by traumatic brain injury. These results suggest that following brain trauma hypertensive patients may be protected from high blood pressure, but are likely to be more prone to cerebral ischemia when blood pressure drops, and therefore require different therapeutic strategies than normotensive patients.Support or Funding InformationThis work was supported by grants from the Marie Curie Actions SMARTER 7th Framework Program of the European Union 606998 (to NSz and AK), the Hungarian Academy of Sciences (the Bolyai Research Scholarship BO/00634/15 to PT), the Hungarian Brain Research Program (Grant No. KTIA_13_NAP‐A‐II/8 to PT, ECz and AB) and the Hungarian Scientific Research Fund (K108444 to AK).

Case Report of Posttraumatic Middle Cerebral Artery Territory Infarct

A 27-year-old man had severe diffuse brain injury. The patient developed malignant right MCA territory infarction on second day. Emergency decompressive craniectomy was done. He was ventilated. He developed subdural hygroma on the opposite side that was drained. He improved slowly. He had hydrocephalus. VP shunt was done. He became conscious but dependent. PEG was done for feeding. Cranioplasty was done for syndrome of trephined. The patent improved to a state of good cognition with residual motor aphasia and left hemiplegia.Posttraumatic cerebral infarction is an indicator of poor prognosis. Vasospasm, intimal dissection, and thrombosis are the mechanisms. MCA territorial infarction is rare. Usual mechanism is impact of rotational forces on relatively fixed M1 segment on the posterior margin of lower wing of sphenoid, resulting in arterial dissection or intimal damage.

Sir Hugh Cairns and World War II British advances in head injury management, diffuse brain injury, and concussion: an Oxford tale.

The authors trace the Oxford, England, roots of World War II (WWII)-related advances in head injury management, the biomechanics of concussion and brain injury, and postwar delineation of pathological findings in severe concussion and diffuse brain injury in man. The prominent figure in these developments was the charismatic and innovative Harvey Cushing-trained neurosurgeon Sir Hugh Cairns. Cairns, who was to closely emulate Cushing's surgical and scholarly approach, is credited with saving thousands of lives during WWII by introducing and implementing innovative programs such as helmets for motorcyclists, mobile neurosurgical units near battle zones, and the military usage of penicillin. In addition, he inspired and taught a generation of neurosurgeons, neurologists, and neurological nurses in the care of brain and spinal cord injuries at Oxford's Military Hospital for Head Injuries. During this time Cairns also trained the first full-time female neurosurgeon. Pivotal in supporting animal research demonstrating the critical role of acceleration in the causation of concussion, Cairns recruited the physicist Hylas Holbourn, whose research implicated rotary acceleration and shear strains as particularly damaging. Cairns' work in military medicine and head injury remain highly influential in efforts to mitigate and manage brain injury.

Severe diffuse brain injury. Justifiability of decompressive craniectomy

Objective: To study the possibility of improvement of response to treatment of injured persons with severe diffuse brain injury (SDBI) through the intracranial pressure (ICP) monitoring and active correction of intracranial hypertension (ICH) with the use of decompressive craniectomy (DC). Material and methods: A prospective analysis of response to treatment of 57 injured persons with SDBI was carried out. The first period of research (2000 – 2005): 34 patients. The second period (2006 – 2012): 23 patients. The main criterion of enrolment to the research is a severe brain injury (8 points or less according GSC scale). L.F. Marshall classification of diffuse injury to brain was used. ICP measurement during the second period was carried using the parenchymal sensors on the monitor Brain Pressure Monitor REF HDM 26.1/FV500 Spiegelberg (Germany). Results: Augmentation of signs of axial and lateral dislocation with the transition from type I to type IV of SDBI of the brain is related to the increased rate of detection and intensity of ICH. ICH was discovered among 25% of patients with type II of SDBI, and among 57% with type III and 80% with type IV of SDBI. Average ICP in the group of injured persons with type II of SDBI constituted (14.4±6.6) mm Hg, with type III – (30±20.6) mm Hg, with type IV – (37.6±14.1) mm Hg. As long as the rate of ICH detection increases, the necessity to use more aggressive treatment methods increases as well, including the DC. DC was not used for type I and type II of SDBI. During the first period, DC was carried out only for 15.4% of injured persons with the injury of type IV. During the second period, DC was carried out for 42.9% of injured persons with type III and for 100 injured persons with type IV of SDBI. The average ICP in the group of injured persons with SDBI, who were subjected to DC, constituted (41±18.6) mm Hg prior to the operation and (20.1±18) mm Hg after the operation. DC fulfillment resulted in ICP reduction by a mean of 46.6%. Lethality during the first observation period constituted 52.9%, and during the second one – 39.1% (χ 2 =10.9; р<0.004). During the first period of research the benign outcome (good recovery + moderate disability according to the Glasgow outcome scale) was achieved among 17.7% of injured persons, and during the second period - among 26% (р<0.05). Conclusions: SDBI types according to L.F. Marshall classification that are determined on the basis of primary CT of brain, correlate with the ICH rate and intensity, lethality rate, and they must be taken into consideration when determining the treatment policy.

Brain activation by music in patients in a vegetative or minimally conscious state following diffuse brain injury

Objective: The aim of this study was to objectively evaluate the brain activity potential of patients with impaired consciousness in a chronic stage of diffuse brain injury (DBI) using functional MRI (fMRI) following music stimulation (MS).Methods: Two patients in a minimally conscious state (MCS) and five patients in a vegetative state (VS) due to severe DBI were enrolled along with 21 healthy adults. This study examined the brain regions activated by music and assessed topographical differences of the MS-activated brain among healthy adults and these patients.Results: MS was shown to activate the bilateral superior temporal gyri (STG) of both healthy adults and patients in an MCS. In four of five patients in a VS, however, no significant activation in STG could be induced by the same MS. The remaining patient in a VS displayed the same MS-induced brain activation in STG as healthy adults and patients in an MCS and this patient’s status also improved to an MCS 4 months after the study.Conclusions: The presence of STG activation by MS may predict a possible improvement of patients in a VS to MCS and fMRI employing MS may be a useful modality to objectively evaluate consciousness in these patients.

Emergence from protracted unconsciousness due to severe diffuse axonal brain injury: clinical observation and literature review

The paper gives data available in the literature on the variants of unconsciousness, bases of their development, and modes of correction. The authors analyze their observation of consciousness recovery after protracted unconsciousness (for about 6 months) during neuromodulation therapy and repetitive transcranial magnetic stimulation (rTMS) in a patient with severe traumatic and, probably, concominant hypoxic brain injury. Over time (within 2 years), they traced neurological and psychic changes, evaluated structural damages by Tl-, T2-weighted, FLAIR, and DTI magnetic resonance imaging, by constructing corticospinal tracts, and cerebral blood flow (computed tomography perfusion), and plasma catecholamines (epinephrine, norepinephrine, and dopamine). The case in question is clinical, instrumental, and laboratory evidence for the efficiency of use of not only direct stimulants of dopaminergic transmission, but also drugs with indirect dopaminergic activity, as well as rTMS for emergence from protracted akinetic mutism in the presence of akinetic-rigid syndrome.

English

BACKGROUND: The management part of patients of diffuse brain injury is always critical and is associated with the high mortality and morbidity. Many prediction model for prognosis evaluation in diffuse brain injury patients have been developed. These prediction models so far has shown no promising role in therapeutic part of management but sensitivity and specificity of such model in detecting outcome has been observed and validated. In our study we have compiled the data of 400 patients with diagnosis of diffuse brain injury and evaluated their predicted outcome based on prediction scoring developed by National Institute of Mental Health and Neurosciences (NIMHANS) in 2003 and observed the actual outcome at the end of one month of observation. MATERIAL &METHODS: The outcomes of 400 patients with severe diffuse brain injury (GCS<8) were analyzed prospectively. On admission their prediction scoring were done based on the NIMHANS prognostic predictive model .Patients with scores of less than zero were graded to have unfavourable outcome. The actual outcomes of the patients at the end of one month were observed – death or persistent vegetative state was grouped in unfavourable outcome whereas patients those who showed improvement with or without disability were said to have favourable outcome. The percentage of unfavourable outcome was measured and the sensitivity, specificity. Predictive value for favourable and unfavourable outcome of the model in our study was measured and compared to the original study of NIMHANS. RESULTS: The sensitivity, specificity, negative and positive predictive value for the model calculated were 71.68, 83.33, 53. 98 and 91.52 respectively which showed the good efficacy of the model in predicting the outcome in our patients of head injury. CONCLUSION: The prognostic model developed by NIMHANS is a good outcome prediction model which can guide towards the prognosis and further intensive care of the patient but at the same time cannot be used to guide initial therapy .Moreover inclusion of MRI findings can improve accuracy of the study as CT Scan may not show obvious changes in thin patient.

Application of Electrophysiologic Techniques in Poor Outcome Prediction Among Patients With Severe Focal and Diffuse Ischemic Brain Injury

To explore various electrophysiologic examinations as predictors for poor outcome in patients with severe ischemic brain injury, by comparing the prognostic ability of EEG, short-latency somatosensory evoked potentials (SLSEP), and brain stem auditory evoked potentials (BAEP). EEG, SLSEP, and BAEP were recorded in 161 patients with severe ischemic brain injuries (Glasgow Coma Scale ≤ 8), 77 with anoxic-ischemic encephalopathy after cardiopulmonary resuscitation, while 84 experienced massive hemispheric infarction at between 1 and 7 days after the onset. Outcomes were reviewed after 6 months using the Glasgow Outcome Scale. Six months after the onset, poor outcomes (Glasgow Outcome Scale, 1-2) were identified in 66 and 54 patients among the anoxic-ischemic encephalopathy and the massive hemispheric infarction group, respectively. By using the prognostic authenticity analysis of predictors, unfavorable EEG patterns, lack of EEG reactivity, pathologic N20 of SLSEP, and pathologic wave V of BAEP showed the high sensitivity (92.4%-97.0%, 95% confidence interval [CI]: 82.5%-99.5%), while bilateral absence of SLSEP N20 showed the highest specificity (100%, 95% CI: 67.9%-100%) and positive predictive value (100%, 95% CI: 90.4%-100%) in the anoxic-ischemic encephalopathy group. In the massive hemispheric infarction group, unfavorable EEG patterns showed the highest sensitivity (96.3%, 95% CI: 86.2%-99.4%) while bilateral absence of SLSEP N20 and BAEP wave V showed the highest specificity (100%, 95% CI: 85.9%-100%) and positive predictive value (100%, 95% CI: 80.8%-100%). The predictive power of electrophysiologic examinations is different according to the etiology of ischemic brain injury. Short-latency somatosensory evoked potentials (N20) can be considered the most powerful method to predict poor outcome in anoxic-ischemic encephalopathy. Combination of EEG (unfavorable EEG patterns) and SLSEP (N20)/BAEP (wave V) is best suited in massive hemispheric infarction to predict poor outcome.

A speech expression disorder in patients with severe diffuse brain injury who emerged from a vegetative or minimally conscious state

Objective: The purpose of this study was to highlight a speech expression disorder considered as a mixed speech apraxia (SA) and dysarthria syndrome in patients with chronic severe diffuse brain injury (DBI) and to determine its correlation with anatomical localizations of brain lesions using neuroimaging.Methods: Among 140 patients with chronic severe DBI, eight showed this type of speech disorder. MRI (five patients) and FDG-PET (six patients) procedures were performed.Results: Affected patients could comprehend verbally, read words silently and express words using a word board. Compared with SA, the disorder is characterized by similarities in regards to reduced phonation and marked facio-oral apraxia, but by distinct differences in terms of an accompanying dysphagia and pyramidal/extra-pyramidal symptoms that are similar to symptoms associated with dysarthria due to pseudobulbar palsy. Diffuse regions of the white matter including the left arcuate fasciculus (AF) were significantly decreased in fractional anisotropy value. However, there was no significant cortical metabolic damage in FDG-PET.Conclusions: The observed speech disorder in these patients is a characteristic entity related to dysfunction of speech expression and may be attributable to damage of not only the AF but also a number of fibres that are related to dysarthria, cognitive and emotional impairments and pyramidal/extra-pyramidal symptoms.

Management and outcome of vein of Galen malformation

ObjectiveTo describe our experience of treating children with vein of Galen aneurysmal malformation (VGM) in a single UK centre between 2003 and 2008.MethodRetrospective review of case notes and neuroimaging.Results33 children...

RESUSCITATION AND CRITICAL CARE OF POOR-GRADE SUBARACHNOID HEMORRHAGE

As outcomes have improved for patients with aneurysmal subarachnoid hemorrhage, most mortality and morbidity that occur today are the result of severe diffuse brain injury in poor-grade patients. The premise of this review is that aggressive emergency cardiopulmonary and neurological resuscitation, coupled with early aneurysm repair and advanced multimodality monitoring in a specialized neurocritical care unit, offers the best approach for achieving further improvements in subarachnoid hemorrhage outcomes. Emergency care should focus on control of elevated intracranial pressure, optimization of cerebral perfusion and oxygenation, and medical and surgical therapy to prevent rebleeding. In the postoperative period, advanced monitoring techniques such as continuous electroencephalography, brain tissue oxygen monitoring, and microdialysis can detect harmful secondary insults, and may eventually be used as end points for goal-directed therapy, with the aim of creating an optimal physiological environment for the comatose injured brain. As part of this paradigm shift, it is essential that aggressive surgical and medical support be linked to compassionate end-of-life care. As neurosurgeons become confident that comfort care can be implemented in a straightforward fashion after a failed trial of early maximal intervention, the usual justification for withholding treatment (survival with neurological devastation) becomes less relevant, and lives may be saved as more patients recover beyond expectations.

An Unusual Cause of Fixed Dilated Pupils After Cardiac Surgery

The presence of fixed, dilated pupils after cardiac surgery is an ominous sign, typically indicating severe diffuse hypoxic-ischemic brain injury. Rarely, however, this finding can be seen as a result of focal midbrain ischemia. It is important to differentiate between these syndromes, as the latter might be amenable to acute stroke treatments, and because they affect consciousness very differently. A 46-year-old man with diffuse atherosclerosis underwent coronary artery bypass grafting and closure of an incidentally discovered patent foramen ovale. He underwent neurologic evaluation on post-operative day 6 because he was not speaking and appeared to have a new right hemiparesis. Eye movements, pupillary, and lid function were all normal at this time. MRI showed multiple posterior circulation infarcts, involving both cerebral peduncles. On post-operative day 12, he became unresponsive, quadriplegic, and had bilaterally fixed, dilated pupils. CT showed low attenuation in nearly the entirety of both cerebral peduncles. Midbrain infarction is rare. Bilateral midbrain infarction is even rarer and typically presents as locked-in syndrome with preservation of pupillary function and at least vertical eye movements. In our review of the literature, we found only three other cases of midbrain infarction associated with bilateral mydriasis. As in our case, these characteristically involved the anteromedial midbrain bilaterally. Fixed, dilated pupils after cardiac surgery can rarely be caused by bilateral anteromedial midbrain infarctions. It is important to differentiate this from the much more common diffuse hypoxic-ischemic injury.

Neuroplasticity following non-penetrating traumatic brain injury

The primary objective of this review is to examine the methodology and evidence for neuroplasticity operating in recovery from traumatic brain injury (TBI), as compared with previous findings in patients sustaining perinatal and infantile focal vascular lesions. The evidence to date indicates that the traditional view of enhanced reorganization of function after early focal brain lesions might apply to early focal brain lesions, but does not conform with studies of early severe diffuse brain injury. In contrast to early focal vascular lesions, young age confers no advantage in the outcome of severe diffuse brain injury. Disruption of myelination could potentially alter connectivity, a suggestion which could be confirmed through diffusion tensor imaging (DTI). Initial reports of DTI in TBI patients support the possibility that this technique can demonstrate alterations in white matter connections which are not seen on conventional magnetic resonance imaging (MRI) and might change over time or with interventions. Preliminary functional MRI studies of TBI patients indicate alterations in the pattern of brain activation, suggesting recruitment of more extensive cortical regions to perform tasks which stress computational resources. Functional MRI, coupled with DTI and possibly other imaging modalities holds the promise of elucidating mechanisms of neuroplasticity and repair following TBI.

Prognostic Factors in Children with Severe Diffuse Brain Injuries: A Study of 74 Patients

Severe diffuse brain injury in children has a devastating influence on their physical and psychological development. This retrospective study was undertaken to analyse the factors that influence outcome in children with such injuries. The short-term outcomes (Glasgow outcome score) of 74 children (age ≤15 years) with severe diffuse brain injury and no focal operable mass lesions on CT scan, admitted between 1992 and 1998 at the National Institute of Mental Health and Neurosciences were analysed. The prognostic factors analysed were age, gender, time after injury to admission, nature of injury, highest post-resuscitation Glasgow coma score (GCS), pupillary reaction, horizontal oculocephalic reflex and CT scan findings. The following factors were found to be independent predictors of poor outcome: GCS 3–5 (p < 0.003), absent verbal response (p < 0.001), motor response score of 1–3 (p < 0.001), absent pupillary reaction (p < 0.001), absent oculocephalic reflex (p < 0.001) and presence of traumatic subarachnoid haemorrhage on CT scan (p < 0.002). These independent variables were then subjected to a stepwise logistic regression analysis, and the most important variables for predicting outcome were oculocephalic reflex and GCS, which together correctly predicted unfavourable outcome with a sensitivity of 79% and a specificity of 65%. An early CT scan or a single CT scan did not have any prognostic significance.

Improved motor outcome in response to magnesium therapy received up to 24 hours after traumatic diffuse axonal brain injury in rats.

The goal of this study was to establish the therapeutic window during which delayed therapy with MgSO4 improves neurological motor outcome in rats that have suffered severe traumatic axonal brain injury. Severe brain injury was induced in male Sprague-Dawley rats by using the impact-acceleration model of severe traumatic diffuse axonal brain injury. Injured animals were subsequently treated with MgSO4 (750 micromol/kg) infused intramuscularly at 30 minutes or at 8, 12, or 24 hours after trauma and were tested for neurological motor outcome during the following week by using the rotarod test. Injured untreated (control) animals demonstrated highly significant (p < 0.001) neurological motor deficits that were sustained over the 1-week assessment period. Animals treated with MgSO4 at 30 minutes or at 8 or 12 hours postinjury demonstrated significantly improved motor outcomes compared with untreated control animals at all time points (0.001 < p < 0.05). Animals treated with MgSO4 at 24 hours had motor scores that were similar to those of untreated control animals early in the week, but demonstrated a significantly more rapid recovery in function and, by the end of the assessment period, they demonstrated significantly improved motor scores (p < 0.01). Repeated administration of MgSO4 over the 1-week observation period did not further improve outcome. The present results demonstrate that Mg++ plays a neuroprotective role following severe diffuse traumatic axonal brain injury. Moreover, Mg++ therapy significantly improved motor outcome when administered up to 24 hours after injury, with early treatments providing the most significant benefit. Repeated administration beyond 24 hours postinjury did not provide additional neuroprotection.

Prognostic factors in postraumatic severe diffuse brain injury.

It is usually defficult in clinical practice to establish factors affecting final outcome in patients suffering severe diffuse brain injury (SDBI), due to the absence of specific semiology. We studied retrospectively 160 consecutive patients with criteria of SDBI. We performed a statistical analysis of epidemiological, clinical and radiological factors, and relationship with final outcome. 35% of patients with severe head injury presented SDBI. Sixty percent were 15-35 year old and 73% male. More than 45% of the patients presented GCS 3 or 4. On CT performed during the first 24 h, haemorrhagic lesions appeared in white matter in 35% and subarachnoid haemorrhage was observed in 28%. During the first 24 h., 66% of patients presented values of intracranial pressure (ICP) above 20 mm Hg and a 33% below 20 mm Hg. Twenty percent of the patients had ICP > 20 mm and no response to treatment. According to the Glasgow Outcome Scale (GOS), mortality of more than 50% and 25% of patients with persistent vegetative state or severe disability were observed. Clinical evaluation, early CT findings, ICP values and their response to medical treatment and clinical complications were found to be related (p < 0.05) to final outcome (GOS).

Does traumatic subarachnoid hemorrhage caused by diffuse brain injury cause delayed ischemic brain damage? Comparison with subarachnoid hemorrhage caused by ruptured intracranial aneurysms.

To examine whether traumatic subarachnoid hemorrhage (TSAH) caused by severe diffuse brain injury leads to delayed ischemic brain damage and secondary deterioration of outcome, as does aneurysmal subarachnoid hemorrhage (ASAH). We examined 99 patients with diffuse brain injury with TSAH and 114 patients with ASAH. Computed tomographic (CT) findings, cerebral blood flow, and neurological outcomes were assessed during the acute and subacute phases and were compared between the two groups. The distribution of subarachnoid hemorrhage on the CT scans differed between the two groups. Unlike ASAH, TSAH was not limited to cisterns surrounding the circle of Willis but extended to supratentorial regions and interhemispheric fissures. Computed tomography-detected subarachnoid hemorrhage disappeared very early with TSAH and gradually with ASAH. In the ASAH group, mean cerebral blood flow decreased to 75% of normal during the acute phase and decreased a further 10% during the subacute phase. In the TSAH group, mean cerebral blood flow decreased to 85% of normal during the acute phase and increased slightly during the subacute phase. Neurological deterioration and in-hospital death peaked on Day 0 in association with TSAH and showed twin peaks in association with ASAH. The incidence of low-density areas on the CT scans was significantly higher with ASAH than with TSAH. All low-density areas on the CT scans of patients with ASAH corresponded to vascular territories, but low-density areas on the CT scans of patients with TSAH were rarely associated with vascular territories and contained deep-seated or gliding contusion types. The findings suggest that the incidence of vasospasm is low in association with TSAH and that the cause is different compared with ASAH. There is no evidence that the presence of TSAH in cases of diffuse brain injury leads to delayed ischemic brain damage and secondary deterioration of outcome.