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Biomedical subjects

H G Hårdemark

Publications and source records attributed to H G Hårdemark.

At least 19 recordsLinked to original sources

The importance of Doppler angle of insonation on differentiation between 50-69% and 70-99% carotid artery stenosis.

AIM: to investigate the importance of Doppler angle differentiating between 50-69% and >/=70% internal carotid artery (ICA) stenosis. MATERIAL AND METHODS: fifty-one patients with a previous diagnosis of 50-69% ICA stenosis (n =53) were re-evaluated by duplex scanning. Spectral Doppler velocity waveforms were obtained from common carotid (CCA), ICA and external (ECA) carotid arteries with the same Doppler angle of insonation as used at the initial duplex scanning, followed by repeated measurements with a fixed 60 degrees angle of insonation. RESULTS: the peak systolic velocity (PSV) in the ICA was 181+/-55 cm/s (mean+/-SD) at the second duplex scanning when the same angle of insonation (mean 46 degrees +/-9) was used as during the initial investigation. When the examination was done with a 60 degrees angle of insonation, PSV ICA was 261+/-96 cm/s (mean+/-SD). In fifteen arteries the estimated degree of ICA stenosis changed from 50-69% to 70-99% due to the application of a fixed Doppler angle of insonation at 60 degrees. CONCLUSION: the Doppler angle of insonation has a significant effect on spectral Doppler velocity measurements. It is crucial that duplex criteria are standardised with a fixed angle of insonation and that this angle is consistently used during velocity estimations.

Carotid Artery, Internal↗

Management and prognostic features of intracerebral hemorrhage during anticoagulant therapy: a Swedish multicenter study.

BACKGROUND AND PURPOSE: Patients treated with oral anticoagulants (ACs) have an increased risk of intracerebral hemorrhage (ICH), which is more often fatal than spontaneous ICH. Options to reverse the AC effect include intravenous administration of vitamin K, plasma, and coagulation factor concentrate. However, the optimal management of AC-related ICH has not been determined in any randomized trial. In this study, the present management of AC-related ICH was surveyed, and determinants of survival were assessed. METHODS: We retrospectively reviewed the medical records of all AC-related ICHs at 10 Swedish hospitals during a 4-year period, 1993 to 1996. Survival status after the ICH was determined from the Swedish National population register. RESULTS: We identified 151 patients with AC-related ICH. Death rates were 53.6% at 30 days, 63.6% at 6 months, and 77.5% at follow-up (mean 3.5 years). The case fatality ratio at 30 days was 96% among patients unconscious on admission (n=27), 80% among patients who became unconscious before active treatment was started (n=15), 55% among patients in whom no special action was taken except withdrawal of AC treatment (n=42), and 28% among patients given active anti-coumarin treatment while they were still conscious (n=64). The case fatality ratio at 30 days was 11% in the group treated with plasma (n=18), 30% in the group treated with vitamin K (n=23), and 39% in the group treated with coagulation factor concentrate (n=23). Within the first 24 to 48 hours after admission, 47% of the patients deteriorated. Choice of therapy to reverse the AC effect differed substantially between the hospitals (P<0.0001), as did the time interval from symptom onset to start of treatment. Multiple logistic regression analysis showed only 2 factors (intraventricular extension of bleeding and ICH volume) that were independently related to case fatality at both 30 days and 6 months. The results were similar when the analysis was restricted to patients who were conscious on admission. CONCLUSIONS: In AC-related ICH, a progressive neurological deterioration during the first 24 to 48 hours after admission is frequent, and the mortality is high. Choice of therapy to reverse the AC effect differed considerably between the hospitals. There was no evidence that any treatment strategy was superior to the others. A randomized controlled trial is needed to determine the best choice of treatment.

Adult↗

Improved survival after aneurysmal subarachnoid hemorrhage: review of case management during a 12-year period.

OBJECT: Based on the concept that unfavorable clinical outcome after aneurysmal subarachnoid hemorrhage (SAH), to a large extent, is a consequence of all ischemic insults sustained by the brain during the acute phase of the disease, management of patients with SAH changed at the authors' institution in the mid-1980s. The new management principles affected referral guidelines, diagnostic and monitoring methods, and pharmacological and surgical treatment in a neurointensive care setting. The impact of such changes on the outcome of aneurysmal SAH over a longer period of time has not previously been studied in detail. This was the present undertaking. METHODS: The authors analyzed all patients with SAH admitted to the neurosurgery department between 1981 and 1992. This period was divided in two parts, Period A (1981-1986) and Period B (1987-1992), and different aspects of management and outcome were recorded for each period. In total, 1206 patients with SAH (mean age 52 years, 59% females) were admitted; an aneurysm presumably causing the SAH was found in 874 (72%). The 30-day mortality rate decreased from 29% during the first 2 years (1981-1982) to 9% during the last 2 years (1991-1992) (Period A 22%; Period B 10%; p<0.0001) and the 6-month mortality rate decreased from 34 to 15% (Period A 26%; Period B 16%; p<0.001). At follow-up review conducted 2 to 9 years (mean 5.2 years) after SAH occurred, patients were evaluated according to the Glasgow Outcome Scale. Subarachnoid hemorrhage-related poor outcome (vegetative or dead) was reduced (Period A 30%; Period B 18%; p<0.001). There was an increase both in patients with favorable outcome (good recovery and moderate disability) (Period A 61 %; Period B 66%) and in those with severe disability (Period A 9%; Period B 16%; p<0.01). CONCLUSIONS: This study provides evidence that the prognosis for patients with aneurysmal SAH has improved during the last decades. The most striking results were a gradual reduction in mortality rates and improved clinical outcomes in patients with Hunt and Hess Grade I or II SAH and in those with intraventricular hemorrhage. The changes in mortality rates and the clinical outcomes of patients with Hunt and Hess Grades III to V SAH were less conspicuous, although reduced incidences of mortality were seen in some subgroups; however, few survivors subsequently appeared to attain a favorable outcome.

Adolescent↗

[Thrombolysis changes the care of stroke].

Thrombolysis using tissue plasminogen activator (tPA) is not the leading strategy in the development of pharmacological treatments for acute ischaemic stroke. The prospect of tPA becoming routine treatment in ischaemic stroke raises several issues the magnitude of the treatment load, the requisite neurological and neuroradiological diagnostic qualifications, identification of local reperfusion effects in the brain, and the pre-hospital and hospital management of acute stroke patients. The results of large randomised trials of intravenous tPA treatment are reviewed in the article, and the current state of our knowledge about interventional thrombolysis is reported. Recruitment for the second European intravenous tPA trail, ECASS II, has recently been completed, and the study findings will be available during the latter half of 1988. In the USA, tPA is already recommended treatment for acute ischaemic stroke within three hours after the onset of symptoms. In Europe, the formulation of guidelines awaits the results of ECASS II.

Cerebral Infarction↗

Spontaneous internal carotid artery dissection. Review.

Spontaneous ICA dissection is an increasingly recognized cause of stroke especially in young adults. The most frequently reported site of involvement is the cervical part of the internal carotid artery (ICA). Although several primary arteriopathies have been related to the development of spontaneous ICA dissection the cause is not clear in most cases. The clinical picture varies from mild cerebral and/or cranial nerve dysfunction to a completed stroke. Angiography has been considered as gold standard in establishing diagnosis. Recently, duplex scanning has emerged as a powerful noninvasive diagnostic tool only in the initial assessment but in the serial follow-up of patients. Early diagnosis is essential as these lesions require anticoagulant treatment. Immediate heparinization is instituted after diagnosis, followed by oral anti-coagulation for at least six months. Surgical treatment is warranted in only few cases. Complete resolutions of the dissection is seen in at least 50% of cases. The risk of recurrent stroke remains low in patients discharged alive after spontaneous ICA dissection.

Adult↗

Intracranial pressure changes following middle cerebral artery occlusion in rats.

Prolonged recording of intracranial pressure (ICP) was performed on rats subjected to middle cerebral artery (MCA) occlusion. ICP was repeatedly recorded before and after occlusion of the vessel via a narrow catheter placed in the cisterna magna. MCA occlusion was followed by an increase in ICP, and a pressure peak occurred after 12-24 h in all animals. Subsequently, essentially two patterns of ICP changes were observed. These seemed to be related to the severity of neurological deficits and extension of the infarct area. In the most severely affected animals, raised ICP was noted throughout the 1st week after MCA occlusion; in rats with reversible neurological deficits, ICP returned to normal values after the first peak at 12-24 h. The present investigation shows that prolonged ICP recording is feasible in MCA-occluded rats. The MCA occlusion model in rats is well characterized. Thus, ICP registration can be used in conjunction with other methods for evaluating treatment against increased ICP.

Animals↗

S-100 protein in cerebrospinal fluid after aneurysmal subarachnoid haemorrhage: relation to functional outcome, late CT and SPECT changes, and signs of higher cortical dysfunction.

The concentration of S-100 protein measured in ventricular cerebrospinal fluid (CSF) from 32 patients with subarachnoid haemorrhage (SAH) during the acute phase was related to features on admission such as the Hunt and Hess neurological scale and the amount of blood at the first computed tomography (CT). The S-100 values were also related to functional outcome assessed by the Glasgow outcome scale (GOS) at 12 months. Twenty-two patients were re-examined more than 2 years after the SAH, and the initial S-100 values were related to signs of structural brain damage at CT and single photon emission computed tomography (SPECT) and to the results of neuropsychological evaluation (NPE). NPE included standardized tests for memory functions, intellectual functions, visuo-spatial abilities, sensory-motor functions, and concept formation. Life-adjustment was assessed by two separate questionnaires. Tests for agnostic dysfunction and the Western aphasia battery test (WABT) were also performed. Patients who were functionally disabled or ultimately died had significantly higher initial CSF concentrations of S-100 protein than patients showing good recovery. Patients with low-attenuated regions and/or increased ventricular size at CT and/or regionally decreased tracer uptake on SPECT had higher S-100 levels during days 2-8 than had patients showing no such changes. Logistic and multiple regression analysis of all characteristics assessed during the acute phase after SAH showed that the CSF S-100 concentration during days 2-8 was the factor best correlated to GOS and findings on CT and/or SPECT. All patients showed varying degrees of cognitive impairment at follow-up. The results of NPE and the WABT were related to outcome assessed by GOS and to increased ventricular size on CT. Women had a stronger feeling of maladjustment, but the scores for life adjustment were otherwise not related to other outcome criteria. It is concluded that the ventricular CSF S-100 concentration during the acute phase after SAH is related not only to the functional outcome as assessed by GOS but also to signs of brain damage seen on late CT and SPECT.

Adult↗

Neurologic and neuropathologic outcome after middle cerebral artery occlusion in rats.

Focal cerebral ischemia was produced in 45 rats by occlusion of the left middle cerebral artery. Groups of rats were investigated over a long period after occlusion, that is, from a few hours to 42 days after the production of focal ischemia. Light microscopy showed infarcts in the frontoparietal cortex and the lateral caudoputamen. The ischemic changes closely resembled those found in ischemic infarcts in humans and followed a similar pattern over time. Measurements of the sizes of the infarct, the ipsilateral (operated) hemisphere, and the contralateral hemisphere from camera lucida drawings revealed that the infarct size changed with time after occlusion. Rats killed during the first 7 days (acute phase) had the largest infarcts; in rats killed thereafter, the infarct size diminished. The size of the ipsilateral hemisphere also changed with time; during the first 7 days after occlusion this hemisphere was swollen and larger than the contralateral hemisphere. We suggest that these acute changes are caused by cerebral edema. After the first 7 days, enlargement of the ipsilateral hemisphere gave way to a significant reduction in the size of both the ipsilateral hemisphere and the infarct. We believe that the major reasons for this shift in size are resorption of fluid together with diminished production of edema and elimination of dead cells by macrophages. We suggest that the amount of tissue loss (i.e., the degree of atrophy and the remaining infarct "scar") found 21-42 days after occlusion (during the late phase) is a measure of the total amount of tissue that succumbed as a consequence of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

S-100 protein and neuron-specific enolase in CSF after experimental traumatic or focal ischemic brain damage.

Cerebrospinal fluid (CSF) markers of brain damage are potentially capable of providing quantitative information about the extent of certain neurological injury. The presence of such markers in CSF after brain damage is transient and it is essential to understand their kinetics if they are to be used in clinical practice. In the present study, the CSF concentrations of two neurospecific proteins. S-100 protein and neuron-specific enolase (NSE), were determined in rats before and repeatedly after one of two types of experimental brain damage: traumatic cortical injury and focal cerebral ischemia induced by middle cerebral artery (MCA) occlusion. The two types of experimental brain damage resulted in significant differences in the kinetics of S-100 and NSE concentrations in CSF. Cortical contusion was followed by a rapid increase in both S-100 and NSE and a peak occurred in both after about 7 1/2 hours, at which time the values declined toward normal. A second, smaller peak was seen after about 1 1/2 days. The increase and decrease in S-100 and NSE levels in CSF was slower after MCA occlusion; a peak was seen after 2 to 4 days. Furthermore, S-100 was generally higher than NSE after trauma, whereas after MCA occlusion the NSE concentration was slightly higher than the S-100 value. These results support the use of CSF markers for estimation of the extent of brain damage in experimental models and forms a basis for the understanding of their kinetics, which is important for their use in clinical practice.

Animals↗

Neuron-specific enolase is a marker of cerebral ischemia and infarct size in rat cerebrospinal fluid.

Neuron-specific enolase concentrations were measured in samples of rat cerebrospinal fluid obtained repeatedly before and after occlusion of the middle cerebral artery. A method for reliable, repeated sampling of cisternal cerebrospinal fluid was developed for this purpose. Occlusion of the middle cerebral artery induced cerebral infarcts of slightly variable size with good correlation to raised neuron-specific enolase concentrations. Sham operation caused only superficial cortical damage at the site of surgery and was followed by an early, slight, and transient increase in neuron-specific enolase concentration. With our technique, the development of cerebral infarcts can be studied in individual rats under experimentally controlled conditions over an extended period of time. Analysis of neuron-specific enolase can be used in trials of drugs for mitigating the effect of ischemia. Information concerning the release of neuron-specific enolase from ischemic cerebral tissue to the cerebrospinal fluid is important because neuron-specific enolase in the cerebrospinal fluid can be determined in patients suffering from cerebrovascular insult.

Animals↗

Influence of clinical factors, CT findings and early management on outcome in supratentorial intracerebral hemorrhage.

BACKGROUND AND PURPOSE: Treatment of supratentorial intracerebral hemorrhage (SICH) is still controversial and new adequately sized randomized controlled trials (RCTs) of surgical evacuation are greatly needed. Our aim was to identify and quantify the most important clinical and CT factors related to prognosis in patients with SICH, to estimate the treatment effect in various subpopulations of surgically treated patients and to make assumptions on target population and sample size in future trials. METHODS: Uni- and multivariate analysis of retrospectively collected data on clinical and CT factors on admission and early management in 203 patients with SICH, mortality at discharge, 30 days, 6 and 12 months and clinical outcome according to the modified Rankin Scale (mRS) at 6 months and follow-up at a mean of 3.1 years after admission. RESULTS: Level of consciousness according to the Glasgow Coma Scale (GCS) and age were the single two factors best related to mortality at 6 and 12 months. GCS and age, in association with hematoma volume and location, arterial hypertension and to some extent use of steroids, were also related to clinical outcome according to the mRS at 6 months and 3.1 years. Surgical evacuation seemed to have a positive effect on clinical outcome in only a small subgroup of the patients. CONCLUSIONS: Our data support a future RCT of surgical evacuation versus conservative treatment in SICH restricted to patients younger than 60-65 years with a GCS on admission in the range of 6-11 and a hematoma not mainly located in the thalamus with a volume in the range of 30-100 ml causing a midline shift of less than 10 mm. Randomization should be balanced within groups of patients with lobar and basal ganglion hematomas, arterial hypertension and intraventricular hemorrhage, and the use of steroids should be discouraged.

Adolescent↗

S-100 protein and neuron-specific enolase in cerebrospinal fluid and serum: markers of cell damage in human central nervous system.

The development of a radioimmunoassay for S-100 protein is described. This method was used in combination with a recently developed radioimmunoassay for neuron-specific enolase in cerebrospinal fluid and serum from 47 patients with cerebral infarction, transient ischemic attack, intracerebral hemorrhage, subarachnoid hemorrhage, and head injury. In cerebrospinal fluid, increased concentrations of both S-100 and neuron-specific enolase were found after large infarcts, whereas after small infarcts and transient ischemic attacks, only neuron-specific enolase increased. The increased concentrations of S-100 and/or neuron-specific enolase were noted 18 hours to 4 days after cerebral infarction and transient ischemic attacks. Cerebrospinal fluid concentrations of these proteins also reflected the severity of the disease in patients with intracerebral hematoma, subarachnoid hemorrhage, or head injury. Temporal changes in serum S-100 and neuron-specific enolase concentrations reflected the clinical course in 4 patients. In stroke patients, the S-100 and neuron-specific enolase concentrations may reflect the extent of brain damage and could be useful in selecting patients with major stroke for more aggressive treatment during the acute phase.

Cerebrovascular Disorders↗