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Biomedical subjects

N A Martin

Publications and source records attributed to N A Martin.

At least 55 records · Page 3Linked to original sources
PubMed1997

Cerebral arterial spasm after penetrating craniocerebral gunshot wounds: transcranial Doppler and cerebral blood flow findings.

OBJECTIVE: The goals of the study were to determine the incidence and time course of cerebral arterial spasm in patients with penetrating craniocerebral gunshot wounds, to study the relationship between vasospasm and subarachnoid hemorrhage (SAH) in these patients, and to evaluate the effects of vasospasm on outcome. METHODS: Thirty-three patients with craniocerebral gunshot wounds underwent computed tomography at admission and then underwent transcranial doppler ultrasonography (TCD). Velocities in the middle cerebral artery and the extracranial internal carotid artery were measured. Vasospasm was defined as a middle cerebral artery velocity greater than 120 cm per second and a hemispheric index (ratio of middle cerebral artery to internal carotid artery velocity) greater than 3. Intravenous xenon-133 cerebral blood flow (CBF) studies were performed for 10 patients. RESULTS: TCD was initiated, on average, 1.1 days after injury; 205 studies (mean, 6.3 studies/patient) were performed 0 to 33 days after injury. TCD showed vasospasm in 14 patients (42.4%). Xenon-133 studies performed within 24 hours of TCD measurements indicating spasm demonstrated normal or low CBF in three of five patients with spasm, ruling out hyperemia as the cause of elevated flow velocities in these three patients. Seven patients had unilateral vasospasm, and seven had bilateral spasm. Vasospasm was most prominent from Days 5 through 11. Vasospasm was distributed across all levels of injury severity, as defined by the Glasgow Coma Scale. Initial computed tomographic scans demonstrated SAH in all 14 patients with vasospasm but in only 9 of 19 without spasm (100 versus 47%, P < 0.0001, binomial distribution probability test). Outcomes for patients with vasospasm were slightly worse than for those without spasm (35.7 versus 47.4% good outcomes, respectively); however, this difference did not reach statistical significance (P = 0.12). CONCLUSION: These findings demonstrate that delayed cerebral arterial spasm is a frequent complication in patients with craniocerebral gunshot wounds and is strongly associated with SAH. The frequency, time course, and severity of spasm are comparable with those observed with aneurysmal SAH and traumatic SAH caused by closed head injury. This study offers new insights into the hemodynamic pathophysiology after gunshot wounds to the brain and suggests that increased vigilance for vasospasm may be of benefit.

Adolescent↗
PubMed1997

Cerebral hyperglycolysis following severe traumatic brain injury in humans: a positron emission tomography study.

Experimental traumatic brain injury studies have shown that cerebral hyperglycolysis is a pathophysiological response to injury-induced ionic and neurochemical cascades. This finding has important implications regarding cellular viability, vulnerability to secondary insults, and the functional capability of affected regions. Prior to this study, posttraumatic hyperglycolysis had not been detected in humans. The characteristics and incidence of cerebral hyperglycolysis were determined in 28 severely head injured patients using [18F]fluorodeoxyglucose-positron emission tomography (FDG-PET). The local cerebral metabolic rate of glucose (CMRG) was calculated using a standard compartmental model. In six of the 28 patients, the global cerebral metabolic rate of oxygen (CMRO2) was determined by the simultaneous measurements of arteriovenous differences of oxygen and cerebral blood flow (xenon-133). Hyperglycolysis, defined as an increase in glucose utilization that measures two standard deviations above expected levels, was documented in all six patients in whom both FDG-PET and CMRO2 determinations were made within 8 days of injury. Five additional patients were found to have localized areas of hyperglycolysis adjacent to focal mass lesions. Within the 1st week following the injury, 56% of patients studied had presumptive evidence of hyperglycolysis. The results of this study indicate that the metabolic state of the traumatically injured brain should be defined differentially in terms of glucose and oxygen metabolism. The use of FDG-PET demonstrates that hyperglycolysis occurs both regionally and globally following severe head injury in humans. The results of this clinical study directly complement those previously reported in experimental brain-injury studies, indicating the capability of imaging a fundamental component of cellular pathophysiology characteristic of head injury.

Adolescent↗
PubMed1997

Cerebral blood flow as a predictor of outcome following traumatic brain injury.

As part of a prospective study of the cerebrovascular effects of head injury, 54 moderate and severely injured patients underwent 184 133Xe-cerebral blood flow (CBF) studies to determine the relationship between the period of maximum blood flow and outcome. The lowest blood flows were observed on the day of injury (Day 0) and the highest CBFs were documented on postinjury Days 1 to 5. Patients were divided into three groups based on CBF values obtained during this period of maximum flow: Group 1 (seven patients), CBF less than 33 ml/100 g/minute on all determinations; Group 2 (13 patients), CBF both less than and greater than or equal to 33 ml/100 g/minute; and Group 3 (34 patients), CBF greater than or equal to 33 ml/100 g/minute on all measurements. For Groups 1, 2, and 3, mean CBF during Days 1 to 5 postinjury was 25.7 +/- 4, 36.5 +/- 4.2, and 49.4 +/- 9.3 ml/100 g/minute, respectively, and PaCO2 at the time of the CBF study was 31.4 +/- 6, 32.7 +/- 2.9, and 33.4 +/- 4.7 mm Hg, respectively. There were significant differences across Groups 1, 2, and 3 regarding mean age, percentage of individuals younger than 35 years of age (42.9%, 23.1%, and 76.5%, respectively), incidence of patients requiring evacuation of intradural hematomas (57.1%, 38.5%, and 17.6%, respectively) and incidence of abnormal pupils (57.1%, 61.5%, and 32.4%, respectively). Favorable neurological outcome at 6 months postinjury in Groups 1, 2, and 3 was 0%, 46.2%, and 58.8%, respectively (p < 0.05). Further analysis of patients in Group 3 revealed that of 14 with poor outcomes, six had one or more episodes of hyperemia-associated intracranial hypertension (simultaneous CBF > 55 ml/100 g/minute and ICP > 20 mm Hg). These six patients were unique in having the highest CBFs for postinjury Days 1 to 5 (mean 59.8 ml/100 g/minute) and the most severe degree of intracranial hypertension and reduced cerebral perfusion pressure (p < 0.0001). These results indicate that a phasic elevation in CBF acutely after head injury is a necessary condition for achieving functional recovery. It is postulated that for the majority of patients, this rise in blood flow results from an increase in metabolic demands in the setting of intact vasoreactivity. In a minority of individuals, however, the constellation of supranormal CBF, severe intracranial hypertension, and poor outcome indicates a state of grossly impaired vasoreactivity with uncoupling between blood flow and metabolism.

Adolescent↗
PubMed1997

Characterization of cerebral hemodynamic phases following severe head trauma: hypoperfusion, hyperemia, and vasospasm.

The extent and timing of posttraumatic cerebral hemodynamic disturbances have significant implications for the monitoring and treatment of patients with head injury. This prospective study of cerebral blood flow (CBF) (measured using 133Xe clearance) and transcranial Doppler (TCD) measurements in 125 patients with severe head trauma has defined three distinct hemodynamic phases during the first 2 weeks after injury. The phases are further characterized by measurements of cerebral arteriovenous oxygen difference (AVDO[2]) and cerebral metabolic rate of oxygen (CMRO[2]). Phase I (hypoperfusion phase) occurs on the day of injury (Day 0) and is defined by a low CBF calculated from cerebral clearance curves integrated to 15 minutes (mean CBF 32.3 +/- 2 ml/100 g/minute), normal middle cerebral artery (MCA) velocity (mean V[MCA] 56.7 +/- 2.9 cm/second), normal hemispheric index ([HI], mean HI 1.67 +/- 0.11), and normal AVDO(2) (mean AVDO[2] 5.4 +/- 0.5 vol%). The CMRO, is approximately 50% of normal (mean CMRO(2) 1.77 +/- 0.18 ml/100 g/minute) during this phase and remains depressed during the second and third phases. In Phase II (hyperemia phase, Days 1-3), CBF increases (46.8 +/- 3 ml/100 g/minute), AVDO(2) falls (3.8 +/- 0.1 vol%), V(MCA) rises (86 +/- 3.7 cm/second), and the HI remains less than 3 (2.41 +/- 0.1). In Phase III (vasospasm phase, Days 4-15), there is a fall in CBF (35.7 +/- 3.8 ml/100 g/minute), a further increase in V(MCA) (96.7 +/- 6.3 cm/second), and a pronounced rise in the HI (2.87 +/- 0.22). This is the first study in which CBF, metabolic, and TCD measurements are combined to define the characteristics and time courses of, and to suggest etiological factors for, the distinct cerebral hemodynamic phases that occur after severe craniocerebral trauma. This research is consistent with and builds on the findings of previous investigations and may provide a useful temporal framework for the organization of existing knowledge regarding posttraumatic cerebrovascular and metabolic pathophysiology.

Adolescent↗
PubMed1997

Intracranial aneurysms treated with the Guglielmi detachable coil: midterm clinical results in a consecutive series of 100 patients.

A prospective study was designed to evaluate clinical outcome in a series of 100 consecutively treated patients who underwent endovascular embolization of 104 intracranial aneurysms using Guglielmi detachable coils (GDCs). Midterm clinical outcome (2-6 years, average 3.5 years) was obtained for 94 patients and was classified according to a modified Glasgow Outcome Scale. Of nine patients treated in the acute phase of severe subarachnoid hemorrhage (Grade IV or V), seven died from the initial hemorrhage, one had a poor outcome, and one had a fair midterm outcome, with no post-GDC embolization hemorrhages. Twenty patients underwent subsequent surgical or endovascular procedures that did not include the use of GDCs. These included aneurysm clipping in nine patients and parent vessel sacrifice in 11 patients. None of these 20 patients experienced post-GDC embolization hemorrhage. The postoperative midterm clinical outcomes of these 20 patients did not significantly differ from the outcomes of patients who underwent GDC embolization as their definitive treatment. Six patients died of unrelated causes prior to reaching the 2-year survival point, with no post-GDC embolization hemorrhage. The midterm outcomes of the remaining 61 patients who underwent GDC embolization as their definitive treatment were classified as excellent (46 patients [75%]), good (seven patients [11%]), fair (three patients [5%]), poor (one patient [2%]), or dead (four patients [7%]). All four patients died from giant lesions. At midterm follow up, the surviving 57 patients' neurological statuses were unchanged or improved in 54 cases and worsened in three cases. The midterm post-GDC embolization hemorrhage rate was 0% for small aneurysms, 4% (one case) for large aneurysms, and 33% (five cases) for giant lesions. The GDC procedure is a safe, effective, and reliable means of preventing aneurysm hemorrhage in patients with small and large intracranial aneurysms. Results, however, are less satisfactory in cases involving giant lesions. Further follow-up review is necessary to establish durability in the longer term. Patients with Grade IV or V subarachnoid hemorrhage in this series generally had poor outcomes even if the GDC procedure was successful in occluding the aneurysm.

Adult↗
PubMed1997

Hemodynamically significant cerebral vasospasm and outcome after head injury: a prospective study.

The authors prospectively investigated cerebral hemodynamic changes in 152 patients with head injuries to clarify the relationship between cerebral vasospasm and outcome. They also sought to determine the most clinically meaningful criteria for diagnosing cerebral vasospasm. Patients with varying degrees of moderate-to-severe head injury were monitored using transcranial Doppler (TCD) ultrasonography and intravenous 133Xe-cerebral blood flow (CBF) measurements. Outcome was determined at 6 months. Using TCD ultrasonography, mean flow velocities were determined for the middle cerebral artery (V(MCA), 149 patients) and basilar artery (V(BA), 126 patients). Recordings of the mean extracranial internal carotid artery velocity (V(EC-ICA)) were also performed to determine the hemispheric ratio (V(MCA)/V(EC-ICA), 147 patients). Cerebral blood flow measurements were obtained in 91 patients. Concurrent TCD and CBF data from 85 patients were used to calculate a "spasm index" (the V(MCA) or V(BA), respectively, divided by the hemispheric or global CBF). The authors investigated the clinical significance of elevated flow velocity, hemispheric ratio, and spasm index. Patients diagnosed as having MCA or BA vasospasm on the basis of TCD-derived criteria alone had a significantly worse outcome than patients without vasospasm. When CBF was considered, hemodynamically significant vasospasm, as defined by an elevated spasm index, was even more strongly associated with poor outcome. Stepwise logistic regression analysis confirmed that hemodynamically significant vasospasm was a significant predictor of poor outcome, independent of the effects of admission Glasgow Coma Scale score and age. On the basis of the results of this study, the authors suggest that the important factor impacting on outcome is not vasospasm per se, but hemodynamically significant vasospasm with low CBF. These findings show that vasospasm is a pathophysiologically important posttraumatic secondary insult, which is best diagnosed by the combined use of TCD and CBF measurements.

Adult↗
PubMed1997

Incidence of cerebral vasospasm after endovascular treatment of acutely ruptured aneurysms: report on 69 cases.

Cerebral vasospasm is the most common cause of morbidity and mortality in patients admitted to the hospital after suffering aneurysmal subarachnoid hemorrhage (SAH). The early surgical removal of subarachnoid clots and irrigation of the basal cisterns have been reported to reduce the incidence of vasospasm. In contrast to surgery, the endovascular treatment of aneurysms does not allow removal of subarachnoid clots. In this study the authors measured the incidence of symptomatic vasospasm after early endovascular treatment of acutely ruptured aneurysms with Guglielmi detachable coils (GDCs). Sixty-nine patients classified as Hunt and Hess Grades I to III underwent occlusion of intracranial aneurysms via GDCs within 72 hours of rupture. The amount of blood on the initial computerized tomography (CT) scan was classified by means of Fisher's scale. Symptomatic vasospasm was defined as the onset of neurological deterioration verified with angiographic or transcranial Doppler studies. Hypertensive, hypervolemic, hemodilution therapy, with or without intracranial angioplasty, was used to treat vasospasm after GDC placement. Symptomatic vasospasm occurred in 16 (23%) of 69 patients. The clinical grade at admission and the amount of blood on the initial CT were both associated with the incidence of subsequent vasospasm. At 6-month clinical follow-up examination, 12 of these 16 patients experienced a good recovery, two were moderately disabled, and two patients had died of vasospasm. In conclusion, the 23% incidence of symptomatic vasospasm in this series compares favorably with that found in conventional surgical series of patients with acute aneurysmal SAH. These results indicate that endovascular therapy does not have an unfavorable impact on cerebral vasospasm.

Acute Disease↗
PubMed1996

Treatment of large and giant fusiform intracranial aneurysms with Guglielmi detachable coils.

Results in nine patients with large or giant fusiform intracranial aneurysms that were treated with Guglielmi detachable coils (GDCs) are reported. There were six males and three females between the ages of 12 and 63. Four patients presented with subarachnoid hemorrhage (SAH) and four with mass effect; in one patient the aneurysm was asymptomatic and located in an arterial feeder of an arteriovenous malformation. Five aneurysms were supratentorial and four were in the posterior fossa. Five were giant and four were large. Selective occlusion with preservation of the parent artery was attempted in three cases, and complete occlusion of the aneurysm and the parent artery was performed in six patients. The tolerance to parent artery occlusion was assessed by angiography, balloon test occlusion, and amytal testing. Six aneurysms were permanently occluded and two partially recanalized. In one case, GDC embolization was not possible. The four patients who presented with SAH made an excellent clinical recovery. Three of the four patients presenting with mass effect recovered completely and one remained unchanged. The patient with an incidental aneurysm remained asymptomatic. There were no permanent complications. In conclusion, GDCs were useful for the occlusion of large and giant intradural fusiform aneurysms. Occlusion of the aneurysm and the parent artery afforded the greatest opportunity for a complete cure. Advantages of GDCs compared to balloons include: occlusion of a shorter segment of normal artery, no traction on the parent vessel, and safer and easier catheterization techniques.

Adult↗
PubMed1996

Hyperemia following traumatic brain injury: relationship to intracranial hypertension and outcome.

The role of posttraumatic hyperemia in the development of raised intracranial pressure (ICP) has important pathophysiological and therapeutic implications. To determine the relationship between hyperemia (cerebral blood flow (CBF) > 55 ml/100 g/minute), intracranial hypertension (ICP > 20 mm Hg), and neurological outcome, 193 simultaneous measurements of ICP and CBF (xenon-133 method) were obtained in 59 patients with moderate and severe head injury. Hyperemia was associated with an increased incidence of simultaneous intracranial hypertension compared to nonhyperemic CBF measurements (32.2% vs. 21.6%, respectively; p < 0.059). However, in 78% of blood flow studies in which ICP was greater than 20 mm Hg, CBF was less than or equal to 55 ml/100 g/minute. At least one episode of hyperemia was documented in 34% of patients, all of whom had a Glasgow Coma Scale (GCS) score of 9 or below. In 12 individuals with hyperemia without simultaneous intracranial hypertension, ICP was greater than 20 mm Hg for an average of 11 +/- 16 hours and favorable outcomes were seen in 75% of patients. In contrast, in eight individuals with hyperemia and at least one episode of hyperemia-associated intracranial hypertension, ICP was greater than 20 mm Hg for an average of 148 +/- 84 hours (p < 0.001), and a favorable outcome was seen in only one patient (p < 0.001). Compared to the remainder of the cohort, patients with hyperemia-associated intracranial hypertension were distinctive in being the youngest, exhibiting the lowest GCS scores (all < or = 6), and having the highest incidence of effaced basilar cisterns and intractable intracranial hypertension. In the majority of individuals with hyperemia-associated intracranial hypertension, their clinical profile suggests the occurrence of a severe initial insult with resultant gross impairment of metabolic vasoreactivity and pressure autoregulation. In a minority of these patients, however, high CBF may be coupled to a hypermetabolic state, given their responsiveness to metabolic suppressive therapy. In patients with hyperemia but without intracranial hypertension, elevated CBF is also likely to be a manifestation of appropriate coupling to increased metabolic demand consistent with a generally favorable outcome. This study supports the concept that there are multiple etiologies of both elevated blood flow and intracranial hypertension after head injury.

Adult↗
PubMed1995

Posttraumatic cerebral arterial spasm.

Posttraumatic cerebral arterial spasm (vasospasm) has been demonstrated in the past by angiography, and recently by transcranial Doppler ultrasonography. Posttraumatic vasospasm is a delayed complication that involves the large basal intracranial arteries (e.g., internal carotid, middle cerebral, basilar) and occurs in 25-40% of head trauma patient. The time course of posttraumatic vasospasm resembles that of vasospasm associated with aneurysmal subarachnoid hemorrhage with onset occurring 2 or more days after injury. A study of the relationship of admission CT scan findings to the incidence of vasospasm suggests that intradural bleeding, which extends into the CSF (subarachnoid, intraventricular, and subdural hemorrhage), plays a role in the pathogenesis of posttraumatic arterial spasm. The preliminary results of a large prospective study of head trauma patients suggest that vasospasm may be an important determinant of outcome from severe head injury.

Brain Injuries↗
PubMed1995

Posterolateral cervical or thoracic approach with spinal cord rotation for vascular malformations or tumors of the ventrolateral spinal cord.

This report describes a technique for exposing the ventrolateral quadrant of the spinal cord through an extended posterolateral approach that can be used in both cervical and thoracic regions. The surgical technique includes the following: 1) a midline skin incision with a transverse extension at the level of pathology; 2) unilateral division and retraction of the paraspinous muscles; 3) laminectomy and unilateral removal of facets and pedicles; 4) dural incision over the dorsal root entry zone; 5) multilevel division of the ipsilateral dentate ligaments; and 6) elevation and rotation of the spinal cord with dentate traction stiches. This technique provides exposure of the ventral root entry zone, the ipsilateral half of the ventral surface of the cord, and the anterior spinal artery. The surface of the spinal cord beyond the anterior spinal artery is not seen. This approach has been used for the treatment of seven ventrolateral spinal cord lesions: five spinal arteriovenous malformations (two Type II, one Type III, two Type IV), one hemangioblastoma, and one cavernous angioma. All the lesions were completely excised. Two patients had mild new neurological deficit after surgery, and one adolescent developed mild asymptomatic thoracic kyphosis, but no other spinal instability was observed over a follow-up period of 1 to 4 years. This operative approach provides significant advantages for ventrolateral perimedullary or intramedullary lesions of the cervical or thoracic spinal cord.

Adolescent↗
PubMed1995

Neurosurgical management of cerebral aneurysms following unsuccessful or incomplete endovascular embolization.

Modern endovascular techniques permit treatment of intracranial aneurysms in many circumstances when surgery is associated with significant morbidity. Occasionally, embolization of aneurysms is unsuccessful or incomplete or followed by complications, in which case surgical management is required. Since 1986, 196 patients have undergone embolization of intracranial aneurysms at the authors' institution and 21 (11%) required subsequent surgical treatment. Attempted embolization failed in five patients (Group A). Ten patients (Group B) had only partial occlusion of the aneurysm or demonstrated recanalization on follow-up studies. Eight of these Group B patients underwent embolization with Guglielmi detachable coils (GDCs), representing 5.7% of the 141 GDC-treated patients in this experience. Surgical treatment in these two groups consisted of clipping (eight cases), surgical parent vessel occlusion (one case), and parent vessel occlusion with extracranial-intracranial bypass (six cases). Fourteen (93%) of the 15 patients in these two groups had an excellent or good outcome with complete aneurysm occlusion. Six patients underwent surgery to treat complications related to the endovascular procedure (Group C). Of these, four patients had neurological improvement compared to their preoperative state, and two died. This series of cases demonstrates that surgical treatment of aneurysms is usually possible with good results following incomplete embolization and emphasizes the need for close and continued neurosurgical involvement in the endovascular management of intracranial aneurysms.

Adult↗
PubMed1995

Cerebral hemodynamic disturbances following penetrating craniocerebral injury and their influence on outcome.

Available data on the subject of cerebrovascular dynamics after penetrating craniocerebral injury and their effect on outcome were reviewed. Following penetrating injury, CBF is depressed, as is cerebral metabolism. This decreased flow likely is associated with poor outcome as previously shown in closed head injuries. A phenomenon interrelated with a decreased blood flow is posttraumatic vasospasm. Vasospasm occurs in a significant percentage of patients as demonstrated both by TCD and angiography, and there is a strong relationship with SAH. Vasospasm following penetrating injury has an onset and time course similar to that seen in both closed head injury and aneurysmal SAH. Vasospasm following penetrating craniocerebral injury may be a cause of secondary ischemic injury, but further study is needed before the prognostic significance of this phenomenon is defined. For now, drawing a parallel with closed head injury and aneurysmal SAH, it can be inferred that vasospasm following cranial gunshot wound may be an important pathophysiologic factor. Because interventions are available to combat vasospasm, including medications (e.g., nimodipine), volume expansion, and elevation of blood pressure, the authors believe that identification and treatment of this potentially damaging condition are compelling, especially in patients whose CT scans demonstrate SAH.

Animals↗
PubMed1994

Metabolic alterations accompany ionic disturbances and cellular swelling during a hypoxic insult to the retina: an in vitro study.

To study the ionic, metabolic, and morphologic derangements that occur following brain injury we utilized a retina in vitro model of hypoxia. Retinas were dissected into oxygenated (95% O2, 5% CO2) Ames medium, a physiologic solution resembling cerebrospinal fluid, and randomly assigned to either experimental hypoxic conditions (95% N2, 5% CO2) or control conditions. All retinas were incubated and maintained at 37 degrees C. Changes in extracellular K+ and lactate concentration, intracellular incorporation of 45Ca and 14C-leucine, uptake of glucose using [14C]-2-deoxy-D-glucose (2DG), and cell size were determined at 10, 20, 30, and 60 minute time intervals. The results show that compared to control retinas hypoxia produced: (1) an early increase in extracellular concentration of K+ and lactate, (2) a delayed increase in the intracellular incorporation of 45Ca, (3) an early onset of cellular swelling, and (4) a decrease in the intracellular incorporation of 14C-leucine, and (5) increased glucose utilization. All of the results were statistically significant (p < 0.05) and exhibited a dose response relationship with the exception of intracellular incorporation of 45Ca which did not become significantly different until 30 minutes post-hypoxia. A 16% increase in cell size was noted after 10 minutes of hypoxia. Increased hypoxic cell size persisted for 30 minutes but after 60 minutes the control retinas appeared enlarged as well. Our results suggest that ionic, metabolic, and morphologic derangements can be demonstrated utilizing an in vitro model of hypoxia which are similar to those seen following in vivo traumatic brain injury. With use of this model the mechanisms behind these ionic-metabolic relationships can be addressed at the molecular level.

Animals↗
PubMed1994

Regional cerebral blood flow trends in head injured patients with focal contusions and cerebral edema.

Focal contusions following head injury may be associated with focal or diffuse cerebral edema. Early global hyperemia and perifocal hyperemia may play a role in cerebral edema, although causal relationships have yet to be clearly been defined. We studied 27 patients with head injury (admission GCS 3-12) resulting in focal contusions (without evidence of subarachnoid, intraventricular or intraparenchymal hemorrhage by CT). Patients were studied with ICP monitors, head CTs, and intravenous 133Xenon regional cerebral perfusion studies serially over several days post injury. Low cortical blood flow and a low mean CBF15 flow were evident on the day of the injury. Additionally, F1 analysis indicated significantly (p < 0.05) greater cortical blood flow in the surrounding brain (mean 60 cc/100 g/min) compared to the contusion area (mean 43 cc/100 g/min) on the day of trauma. Mean regional CBF remained below normal in the contused areas (CBF15 < 35 cc/100 g/min), however the cortical flow increased in the first few days post-injury (peak F1 = 95 cc/100 g/min on day 3) then decreased to sub-normal levels. The mean CBF in the surrounding brain was low on the day of injury (CBF15 = 29 cc/100 g/min), although higher than the contused area, and increased to a peak of 45 cc/1009/min on day 3 posttrauma. Cortical flow in the surrounding brain, however, exhibited a different trend. The mean F1 was low on the day of trauma and significantly higher one day after trauma (mean 105 cc/100 g/min). Only 15 of the 27 patients with focal contusions had evidence of cerebral edema. Eleven of these exhibited focal edema and 4 exhibited diffuse edema. Focal edema developed over the first few days posttrauma as seen in followup CT, whereas patients with diffuse edema exhibited edema on the admission CT. Initial oligemia in the contused areas was associated with a subsequent hyperemic rim about the contusion. Focal hyperemia was associated with focal edema in 41% of the patients, whereas diffuse edema appeared to be independent of the hyperemic response in contusions.

Adolescent↗
PubMed1994

A comparison of quantitative electroencephalography, computed tomography, and behavioral evaluations to localize impairment in patients with stroke and transient ischemic attacks.

Brain computed tomography and a structured behavioral assessment provided a better correlation than did quantitative electroencephalography to the presence of mild stroke or transient ischemic attacks in 21 patients. When electroencephalography did not correlate well, it tended to localize too laterally or miss deep lesions. Computed tomography did not identify 2 lesions when done early after disease onset. No test was uniformly more sensitive or accurate than others. They may complement each other.

Activities of Daily Living↗
PubMed1994

Localization of motor areas adjacent to arteriovenous malformations. A positron emission tomographic study.

Motor cortex activity was localized with positron emission tomography (PET) in 4 patients with large arteriovenous malformations adjacent to or undercutting the left primary motor cortex. Relative cerebral blood flow responses were measured during execution of a visually guided motor tracking task performed with the right index finger, hand, great toe, tongue, or eyes alone (control) and mapped onto each patient's corresponding magnetic resonance imaging (MRI) scan. The relative cerebral blood flow responses in the contralateral precentral gyrus, adjacent to each arteriovenous malformation, demonstrated a normal somatotopic distribution, similar to that in a control population. In the 3 patients with preserved motor function, responses were also present in the ipsilateral primary motor cortex, bilateral supplementary motor area, and ipsilateral anterior cerebellum, similar in location to those of a control population. In the fourth patient with a hemiparesis, responses were attenuated in the primary motor cortex, increased in the supplementary motor area, and absent in the cerebellum. The results demonstrate that PET cerebral blood flow mapping can localize motor cortex despite the presence of significant blood flow abnormalities in adjacent arteriovenous malformations. The method, particularly when combined with MRI, may be used in the planning of surgical, radiation, or embolization therapy.

Adult↗