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Cerebrovascular trauma includes a wide variety of injuries, including dissections, traumatic aneurysms, arteriovenous fistulas, and vascular occlusions. These entities, which are often underdiagnosed, can produce devastating neurologic complications. This article reviews the clinical and radiographic presentations of vascular trauma to increase awareness of these injuries and improve our ability to detect and treat them.
Cerebrovascular trauma is a heterogeneous group of injuries including arterial dissections, traumatic aneurysms, arteriovenous fistulas, and venous occlusions. Detection of vascular trauma may be difficult because of variations in clinical presentation; however, in recent years, increased awareness and understanding of these injuries has improved the ability to detect and subsequently treat many lesions. Despite advances in other imaging modalities, angiography remains the primary radiographic tool used in the evaluation of traumatic vascular lesions.
Trauma to the cerebrovascular system can result in vascular injuries, such as dissection, pseudoaneurysm, thrombosis, rupture, and arteriovenous fistula. Although the diagnosis of vascular injury is usually considered in all cases of penetrating trauma, it may be overlooked in patients with nonpenetrating trauma. The possibility of vascular injury should be considered in all patients with head and neck trauma, especially those patients with acute or delayed neurologic dysfunction. Although intra-arterial angiography remains the gold standard diagnostic tool, the combination of MR imaging and MR angiography may permit noninvasive diagnosis of vascular injury. Moreover, MR readily provides detection of intracranial sequelae, such as cerebral infarction and intracranial hemorrhage.
The term "frontal lobe syndrome" comprises a variety of different clinical syndromes produced by focal lesions involving the prefrontal cortex. However, similar syndromes can be observed after lesions involving subcortical structures connected with the prefrontal cortex in neuronal networks. With respect to the different clinical pictures and underlying brain lesions, prefrontal lobe dysfunction may be divided into a disorganized type, caused by lesion of the dorsolateral prefrontal lobe and its connections, a disinhibited type that can be observed following lesions of the orbitofrontal cortex, and an apathetic type following lesions affecting the functional balance between the cingulum and the supplementary motor area. As intracerebral lesions are rarely limited to the brain regions described, in the majority of patients various degrees of behavioural dysfunction can be observed. The case reports of four patients illustrating the three major prefrontal syndromes following severe head injury (n = 2) or cerebrovascular disease (n = 2) are presented and diagnostic implications as well as possible treatment strategies are discussed.
It appears that the expression of vascular endothelial growth factor (VEGF) is increased during brain injury and thus may contribute to disruption of the blood-brain barrier (BBB) during cerebrovascular trauma. The first goal of this study was to determine the effect of VEGF on permeability of the BBB in vivo. The second goal was to determine possible cellular mechanisms by which VEGF increases permeability of the BBB. We examined the pial microcirculation in rats using intravital fluorescence microscopy. Permeability of the BBB [clearance of FITC-labeled dextran of molecular mass 10,000 Da (FITC-dextran-10K)] and diameter of pial arterioles were measured in absence and presence of VEGF (0.01 and 0.1 nM). During superfusion with vehicle (saline), clearance of FITC-dextran-10K from pial vessels was minimal and diameter of pial arterioles remained constant. Topical application of VEGF (0.01 nM) did not alter permeability of the BBB to FITC-dextran-10K or arteriolar diameter. However, superfusion with VEGF (0.1 nM) produced a marked increase in clearance of FITC-dextran-10K and a modest dilatation of pial arterioles. To determine a potential role for nitric oxide and stimulation of soluble guanylate cyclase in VEGF-induced increases in permeability of the BBB and arteriolar dilatation, we examined the effects of NG-monomethyl-L-arginine (L-NMMA; 10 microM) and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 1.0 microM), respectively. L-NMMA and ODQ inhibited VEGF-induced increases in permeability of the BBB and arteriolar dilatation. The findings of the present study suggest that VEGF, which appears to be increased in brain tissue during cerebrovascular trauma, increases the permeability of the BBB via the synthesis/release of nitric oxide and subsequent activation of soluble guanylate cyclase.
Our ability to identify cerebrovascular lesions in children has improved in recent years and with it our willingness to consider the diagnosis of cerebrovascular disease in children. Magnetic resonance angiography and other tests have made diagnosis easier and safer, particularly in very young children and in patients with sickle cell disease. Transcranial Doppler examination makes it possible to accurately predict without angiography which patients with sickle cell disease are at most risk for stroke. Many patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS) syndrome have a specific mutation of the mitochondrial DNA, and soon the recently devised diagnostic criteria for MELAS syndrome may be replaced by molecular markers. There are many causes of cerebrovascular disease in children, and a thorough evaluation will discover a likely cause in about two thirds of the patients. Recent attention has focused on the HLA-B51 antigen and chicken pox as possible risk factors. Magnetic resonance imaging is also helpful in assessing the prognosis of children with cerebrovascular disease or head trauma.
Thirty-eight patients in coma due to head trauma, cerebrovascular accidents, hypoxia, hypoglycaemia, or barbiturate intoxication, and 15 cases of brain death were studied. Cerebral metabolic rate of oxygen (CMRO(2)) was obtained from the arteriovenous oxygen difference and cerebral blood flow (CBF) measured by intra-arterial (133)Xenon method. If hypothermia and CNS depressants were excluded, CMRO(2) below one-third of normal was incompatible with regaining of consciousness, but this was seen in only three comatose patients. Irrespective of the clinical outcome (death, vegetative survival, or recovery), CMRO(2) values of one-third to two-thirds of normal were seen in the majority of coma patients. CMRO(2) measurements were of no practical value to predict the prognosis in coma, even when the effect of temperature and sedatives were considered. In brain death the CBF studies gave indirect evidence of cerebral circulatory arrest. The cerebrospinal fluid (CSF) was obtained for analysis of lactate, pyruvate, and bicarbonate in 29 cases. Increased CSF lactate levels were found in all groups except barbiturate intoxication. The finding of a negative correlation between CSF bicarbonate and log CBF suggests that the CSFpH determines the wide range of CBF in coma.
The temporal bones of a 2-year-old child who had drowned were examined histopathologically. The abnormalities were limited to the submucosa and lumen of the tympanomastoid space. Abnormalities included severe edema, vascular congestion, and focal ecchymosis without inflammation in the submucosa and hemorrhage into the tympanomastoid air space. To determine the incidence of tympanomastoid hemorrhage in autopsy material, 258 temporal bones were reviewed, and 11 were found to have free blood in the tympanomastoid space. When specimens from victims of skull fractures, cerebrovascular accidents, and leukemia were excluded from the 11, the only specimen remaining was found to be that from a drowning victim. Tympanomastoid hemorrhage in the absence of otitis media, head trauma, cerebrovascular accident, or a bleeding diathesis appears to be strong supporting evidence for death by drowning.
During a three-year period 77 patients (43 men and 34 women, aged 21-82 years, mean age 62.0 years) were treated with mechanical ventilation in a medical intensive care unit. Three patients were treated twice. The most common diagnoses (in decreasing order of frequency) were acute exacerbation of chronic obstructive pulmonary disease, acute myocardial infarction, cerebrovascular trauma and chronic ischemic cardiac disease. The mean duration of ventilation was 6.4 days. 41 patients (51.3%) survived--80% of whom could be discharged to their home. Patients with chronic pulmonary disease showed the highest survival rate, those with cerebrovascular disease the lowest, with the cardiac patients in-between. It is calculated that it cost NOK 207,000 to treat each patient who survived.
More than one-third of patients diagnosed with head injury are intoxicated with ethanol. Most clinical and animal studies have shown alcohol to have a deleterious impact in the setting of cerebrovascular trauma; however, there are also data showing neuroprotective effects in low ethanol doses. Human studies using imaging modalities suggest that small doses of alcohol produce cerebral vasodilatation and higher doses cerebral vasoconstriction. The aim of this study was to investigate the effect of ethanol intake on dynamic cerebral autoregulation and velocities in the middle cerebral arteries, and compare these changes with the effects of hypercapnia. Dynamic cerebral autoregulation and cerebral blood flow velocities were analysed before and after alcohol intake (1.1 g/kg of body weight) in six adult volunteers. Cerebral blood flow velocities in both middle cerebral arteries were monitored continuously by transcranial Doppler. A value for dynamic cerebral autoregulation was calculated from the rate of increase in middle cerebral artery velocities after a rapid-step decrease in arterial blood pressure. A sudden decrease in blood pressure was achieved by the release of previously inflated large blood pressure cuffs around the subject's thighs. Three volunteers were also tested before alcohol intake with CO(2) challenge (breathing 6% CO(2)) during the autoregulation procedure. Blood alcohol level reached 90 mg/dl approximately 60 min after ethanol ingestion. Cerebral blood velocities increased by 8% from baseline for uncorrected end-tidal (et) CO(2) and by 24% for correction to et CO(2)=40. Dynamic cerebral autoregulation measured as an autoregulation index decreased from 4.3+/-1.3 to 2.9+/-1.1 (p=0.089), which did not reach statistical significance. During hypercapnic conditions, dynamic cerebral autoregulation dropped from 4+/-0.8 to 0.9+/-0.9. In conclusion, mild alcohol intoxication caused cerebral vasodilatation with a subsequent increase in cerebral blood flow of 8-24%. Dynamic cerebral autoregulation was not found to be significantly impaired by ethanol. Hypercapnia almost completely destroys the physiological autoregulatory mechanism. A mild hyper-ventilation to etCO(2)=34-36 may be a compensatory contra-measure for ethanol-induced vasodilatation in the setting of head trauma.
The first goal of the present study was to determine the effect of tumor necrosis factor-alpha (TNF-alpha) on the permeability of the blood-brain barrier in vivo. The second goal of this study was to investigate cellular pathways responsible for changes in permeability of the blood-brain barrier in response to TNF-alpha. We examined the pial microcirculation in rats using intravital fluorescence microscopy. Permeability of the blood-brain barrier was quantitated by calculating the clearance of fluorescent-labeled dextran (mol. wt=10,000; FITC-dextran-10K) during superfusion with vehicle, tumor necrosis factor (TNF-alpha; 10 ng/ml), TNF-alpha in the presence of an inhibitor of soluble guanylate cyclase (ODQ; 1.0 microM), and TNF-alpha in the presence of an inhibitor of protein tyrosine kinase (genistein; 10 microM). During superfusion with vehicle, clearance of FITC-dextran-10K from pial vessels remained relatively constant during the experimental period. In contrast, superfusion with TNF-alpha markedly increased clearance of FITC-dextran-10K from the cerebral microcirculation. Topical application of ODQ and genistein, significantly inhibited increases in permeability of the blood-brain barrier to FITC-dextran-10K during application of TNF-alpha. Thus, TNF-alpha increases the permeability of the blood-brain barrier to a moderately sized molecule via a mechanism which appears to involve activation of soluble guanylate cyclase and protein tyrosine kinase. In light of evidence suggesting that TNF-alpha production is increased during cerebrovascular trauma, we suggest that the findings of this study may contribute to our understanding of the pathogenesis of disruption of the blood-brain barrier during brain trauma and inflammation.
36 patients with severe neurological diseases (craniocerebral trauma, cerebrovascular insufficiency, meningo-encephalitis, polyneuropathy, paraplegia, intoxication etc.) received for more than 3 months monosaccharides and polyols (Triofusin E 1000) and a 10-%-concentration of crystalline amino acids (Aminofusin L10% kohlenhydratfrei) via the parenteral route in combination with / or exclusively a nutrient-defined diet (Biosorb). Exclusive enteral nutrition was given preference if possible. Numerous laboratory parameters, as for example blood counts, "hepatic enzymes", electrolytes, trace elements, plasma proteins, lipids, urea and creatinine were determined once a week. Substitutions and secondary complications were registered in addition. Iron and plasma proteins had to be substituted most frequently. It could be proved that hypoferremia was caused by insufficient iron supply in case of exclusive/prevailing parenteral nutrition, incorrect application of the iron preparations, inflammatory complications with iron moving into the R.E.S., as well as malabsorption syndromes probably induced by bacteria. Inflammatory complications were also the major cause of protein deficiency syndromes (hypoalbuminemia). In case of relatibely often occurring diarrhea, however, it could clearly be proved that it was not induced by nutrition but was produced by a broad-spectrum antibiosis. Chronically persistent diarrhea with colitis-like colonic changes required enteral feeding with an oligopeptide diet (z.B. Peptisorb) via jejunal feeding tube. Nitrogen balances which were determined after more than 3 months of artificial nutrition formed the basis of a nutritional plan differentiated according to diagnostic groups and stages of disease.
Functional hemispherectomy, indicated for the control of pharmacologically refractory seizures, has been used at the Montreal Neurological Hospital since 1974. We have used this technique in 18 children suffering from intractable seizures secondary to conditions such as infantile hemiplegia, chronic encephalitis, head trauma, cerebrovascular accident, brain dysplasia and Sturge-Weber angiomatosis. None has developed superficial cerebral hemosiderosis often seen following the classical anatomical hemispherectomy. Eighty-two per cent (82%) of patients have been seizure-free since hospital discharge while another 11.5% have had at least 80% reduction in their seizure frequency. Most patients have shown an improvement in their intellectual capacity and sociability.
Spasticity occurs in children and adults due to a wide range of conditions, including cerebral palsy, head and spinal cord trauma, cerebrovascular accidents and multiple sclerosis. Multiple treatment options have been described, including medical and surgical treatments. Medical treatments include intramuscular botulinum A toxin, oral baclofen and supportive bracing. Surgical approaches include selective posterior rhizotomy, intrathecal baclofen and orthopedic procedures to address deformities. Many reports have been published on these different treatment options, but rarely has a comparison been made between them. Therefore, this review is aimed at comparing selective posterior rhizotomy and intrathecal baclofen injection for spasticity due to cerebral palsy, especially in children.
Seizures and epilepsy are common sequelae of acute brain insults such as stroke, traumatic brain injury, and central nervous system infections. Early, or acute symptomatic, seizures occur at the time of the brain insult and may be a marker of severity of injury. A cascade of morphologic and biologic changes in the injured area over months to years leads to hyperexcitability and epileptogenesis. After a variable latency period, late unprovoked seizures and epilepsy occur. The latent period may offer a therapeutic window for the prevention of epileptogenesis and the development of unprovoked seizures and epilepsy. Administration of anticonvulsant drugs following acute brain insults has thus far failed to prevent late epilepsy. Proper choice of disease models and target populations will aid in the development of putative antiepileptogenic agents. The incidence, timing, and pathophysiology of common epileptogenic brain injuries, including head trauma, cerebrovascular disease, brain tumors, neurosurgical procedures, neurodegenerative conditions, status epilepticus, and febrile seizures, are reviewed.
Regional cerebral blood flow (rCBF), cerebral intraventricular pressure (IVP), systemic arterial blood pressure, and cerebral ventricular fluid (CSF) lactate and pH were studied repeatedly in 23 patients during the acute phase of severe brain injury lasting from 3 to 21 days after the trauma. Cerebrovascular autoregulation was tested repeatedly by means of angiotensin infusion in 21 of the patients, and CO2 response in 14 by means of passive hyperventilation. The pressure in the brain ventricles was measured continuously in all patients and kept below 45 mm Hg during the study. If the IVP increased more than 10 mm Hg during the angiotensin infusion (as in one case), the autoregulation test was considered contraindicated and the angiotensin infusion was discontinued. Dissociation between cerebrovascular autoregulation and CO2 response was a common phenomenon. Typically, autoregulation appeared preserved in the most severely injured areas of the cerebral cortex when the patient was deeply comatose, but deteriorated concomitantly with recovery; by the time the patient became alert, the autoregulation was always impaired. The CO2 response was impaired only in patients who were deeply comatose and had attacks of decerebrate rigidity; during recovery the CO2 response became normal. Thus, preserved autoregulation associated with imparied CO2 response indicated very severe brain damage, whereas impaired autoregulation associated with preserved CO2 response suggested moderate or severe brain damage in recovery. These paradoxical observations raise the question whether the preserved autoregulation seen in severely injured brain tissue is a true autoregulation caused by an active vasoconstrictor response to an increase in blood pressure.
A retrospective evaluation of the Computed Tomography (CT) findings in three hundred and forty-four patients with seizures, presenting over a one-year period, was carried out to determine the value of this examination in the assessment of these patients. Eighty-four per cent of patients had non-contrast studies only. Of the remaining patients, two had contrast studies only and the rest had both non-contrast and contrast studies. All cerebral abnormalities detected on contrast studies were evident on non-contrast scans. Forty-two per cent of all patients presenting with seizures were found to have a demonstrable abnormality on CT. There was a greater detection rate in patients with seizures secondary to trauma, cerebrovascular incidents, infection, metabolic causes and suspected tumours. Computed tomography continues to have a place in the evaluation of certain types of seizure patients. The routine use of intravenous contrast does not appear to be justifiable.
174 subjects suffering from late onset epilepsy were examined. The incidence of cerebral atrophy, defined with objective criteria on CT scans by means of a comparative analysis with a matched for age control group was 37.9%. Head traumas, cerebrovascular disorders and alcoholism were the presumed etiological factors in most of the cases while in 25 subjects (20%) the etiology of cerebral atrophy remained unknown ("cryptogenous atrophy"). Clinical profil, psychometric performance and EEG characteristics of these subjects were investigated and compared with the remainder groups of late-onset epileptics. The results obtained show that the subjects with cryptogenous atrophy behave, as regard the features considered, as the late-onset epileptics with normal CT but present an higher familial prevalence for epilepsy. On the contrary they differs in various ways from late-onset epileptics with atrophy of known origin and from epileptics with focal lesions.