Low cerebral blood flow and perfusion reserve induce hyperperfusion after surgical revascularization: case reports and analysis of cerebral hemodynamics

BACKGROUND: Hyperperfusion syndrome after surgical revascularization is a rare complication and there has not been any systematic study on factors that induce hyperperfusion after surgery. In this paper, we retrospectively analyzed the factors related to this syndrome. PATIENTS AND METHODS: We performed 46 cases of surgical revascularization including 33 cases of carotid endarterectomy (CEA) and 13 cases of superficial temporal artery-middle cerebral artery (STA-MCA) anastomosis during the past 5 years. Among these, we encountered three cases of hyperperfusion syndrome despite well-controlled blood pressure postoperatively. To evaluate factors related to the occurrence of hyperperfusion syndrome, we examined four parameters: (1) regional cerebral blood flow (rCBF), (2) the increase in the ratio of the postoperative rCBF compared to the preoperative rCBF (increase ratio), (3) cerebral perfusion reserve presented by the increase of rCBF after acetazolamide administration (delta rCBF), and (4) the difference in mean blood pressure between the preoperative and postoperative state (delta BP). RESULTS: Preoperative rCBF was significantly lower in cases of hyperperfusion syndrome than the control cases (p < 0.01 Mann-Whitney U-test). Moreover delta rCBF was evidently lower in the hyperperfusion cases than the control (p < 0.05 Fisher's exact method). However, there was no significant difference in the delta BP between the hyperperfusion cases and the control cases. CONCLUSION: In cases of marked low perfusion (low rCBF) with poor perfusion reserve (low delta rCBF), hyperperfusion after surgical revascularization can occur even if blood pressure is adequately controlled.     

Ictal cerebral blood flow in seizures originating in the posterolateral cortex

In selecting patients for epilepsy surgery, it is important to distinguish mesial temporal seizures from seizures originating in the posterolateral cortex. We studied ictal cerebral perfusion in five patients with complex partial seizures with clear posterior EEG ictal onsets and clinical seizures semiology suggesting seizure origin in the posterolateral cortex. METHODS: Ictal SPECT was performed during video EEG monitoring using 99mTc-HMPAO as a cerebral perfusion tracer and a rotating gamma camera to acquire images. RESULTS: Three patterns of ictal hyperperfusion were seen: pattern A = temporoparieto-occipital junction extending into the lateral temporal cortex, involving the mesial temporal cortex and basal ganglia to a lesser degree and a small area of hyperperfusion in the contralateral parietal cortex (two patients); pattern B = pattern A but with no hyperperfusion of the mesial temporal cortex (one patient); and pattern C = localized hyperperfusion in the area of the temporoparieto-occipital junction (two patients). CONCLUSION: Our results suggest distinct patterns of ictal perfusion in seizures with posterolateral ictal EEG onsets. Ictal SPECT may be useful in distinguishing such seizures.     

Cerebral hyperperfusion syndrome following carotid endarterectomy

Three patients with a severe symptomatic carotid stenosis developed headache, epileptic seizures and focal neurologic deficits several days after carotid endarterectomy. CT of the brain revealed hypodensities, indicative of cerebral oedema with haemorrhagic components. This is caused by cerebral hyperperfusion, a complication after carotid endarterectomy as a result of increased cerebral perfusion on the side of the operated carotid stenosis. Dysfunction of the cerebral autoregulation believed to be the cause of this hyperperfusion. Sometimes these complications are incorrectly attributed to one of the better known types of stroke.     

Postoperative hyperperfusion in dural arteriovenous fistula associated with venous ischemia: case report

BACKGROUND: It is well known that carotid endarterectomy and extracranial-intracranial arterial bypass sometimes cause postoperative hyperperfusion, and vasoparalysis attributable to long-standing ischemia has been suggested as the cause. It is also well known that dural arteriovenous fistula (AVF) sometimes causes cerebral ischemia attributable to venous hypertension. However, there are few reports regarding the postoperative changes of regional cerebral blood flow (rCBF). METHODS: We report a case of dural AVF of the left transverse/sigmoid sinuses, occurring in a 64-year-old man. Intraoperative transvenous embolization combined with transarterial embolization was performed, and the rCBF was measured pre- and postoperatively using 99mTc-hexamethyl-propylene amine oxime and single-photon emission computed tomography (SPECT). RESULTS: Preoperative SPECT disclosed a marked rCBF reduction in the left temporal, parietal, and occipital lobes. Complete obliteration of the AVF was attained after the intraoperative transvenous embolization, without any neurological deterioration. However, postoperative SPECT demonstrated temporary hyperperfusion in these regions. CONCLUSIONS: Sudden resolution of venous ischemia can lead to postoperative hyperperfusion, and pre- and post-treatment rCBF studies are important to prevent complications related to hyperperfusion.     

Ictal single photon emission computed tomography in occipital lobe seizures

PURPOSE: Ictal single photon emission computed tomography (SPECT) has been evaluated as an adjunctive localizing technique in temporal lobe epilepsies and, to a lesser degree, in some extratemporal epilepsies. The purpose of this study was to determine whether occipital lobe seizures are associated with distinctive ictal cerebral blood perfusion (rCP) patterns. METHODS: SPECT was used with the tracer 99mTc HMPAO to image ictal rCP in 6 patients in whom clinical, EEG, and imaging data indicated occipital lobe seizures. RESULTS: Two patterns of rCP were seen. Four patients had hyperperfusion that was restricted to the occipital lobe, and two patients had hyperperfusion of the occipital lobe and the ipsilateral mesial temporal lobe, with hypoperfusion of the lateral temporal lobe. The latter 2 patients had clinical and surface EEG evidence of temporal lobe involvement in the seizure discharge. CONCLUSIONS: Ictal rCP patterns in occipital lobe seizures are distinct from those in temporal lobe seizures and may vary according to whether or not ipsilateral temporal lobe structures are involved in the ictal discharge.     

Correlation of positive symptoms exclusively to hyperperfusion or hypoperfusion of cerebral cortex in never-treated schizophrenics

BACKGROUND: Studies of schizophrenia by single photon emission computed tomography (SPECT) and positron emission tomography (PET) have shown both regional cerebral hyperperfusion and hypoperfusion. The aim of this study was to examine the inter-relations between regional cerebral blood flow (rCBF), psychopathology, and effects of neuroleptic therapy. METHODS: 24 never-treated patients with acute schizophrenia were examined with hexamethylpropyleneamine-oxime brain SPECT and assessed psychopathologically according to the positive and negative syndrome scale; they were studied again after neuroleptic treatment and psychopathological remission. rCBF values that deviated from those of 20 controls by more than 2 SD were regarded as abnormal. FINDINGS: Both hyperperfused and hypoperfused patterns were found among schizophrenia patients during acute illness. The seven positive symptoms on the symptom scale showed different correlations with rCBF: formal thought disorders and grandiosity correlated positively (and strongly) with bifrontal and bitemporal rCBF; delusions, hallucinations, and distrust correlated negatively (and strongly) with cingulate, left thalamic, left frontal, and left temporal rCBF. Stereotyped ideas as a negative symptom correlated negatively (and strongly) with left frontal, cingulate, left temporal, and left parietal rCBF. After neuroleptic treatment (and reduction of positive symptoms), only negative symptoms correlated exclusively with bifrontal, bitemporal, cingulate, basal ganglia, and thalamic hypoperfusion. INTERPRETATION: Different positive symptoms are accompanied by different rCBF values--some related to hyperperfusion, others to hypoperfusion. This finding may help to explain observed inconsistencies of perfusion patterns in drug-na?ve schizophrenics.     

Mesial temporal sclerosis (II): clinical features and complementary studies

OBJECTIVE: To collect clinical data and diagnostic characteristics of the mesial temporal sclerosis syndrome (MTS). Development. CLINICAL FEATURES: In MTS repeated temporal lobe seizures, difficult to control pharmacologically, are seen in patients with neuropsychological defects which can be shown by appropriate tests. There is no pathognomonic clinical data. However, there is frequently: 1. Onset of seizures during childhood (6-10 years old). 2. Presence of some type of aura. The only significantly related types are visceral, olfactory and uncinate. 3. A pattern of conduct typical of ictus, although this is nonspecific: Early ipsilateral manual automatism and contralateral tonic posture. 4. Infrequent generalization. Surface EEG: Acute elements and/or slow waves in interictal recordings localized to the anterior temporal region, either unilateral or bilateral and with independent expression. MR of encephalum: Two typical ipsilateral findings at the electric focus of independent presentation and not mutually exclusive: a) Hippocampal hyperdensity in T2 sequences. b) Atrophy of hippocampal structures. FDG-PET: Interictal pattern of ipsilateral temporal hyperperfusion with typical maximal involvement of the polar region. SPECT-HMPAO: Early ictal and post-ictal pattern of ipsilateral temporal hyperperfusion. CONCLUSIONS: MTS is a clinical syndrome with its own identity from the clinical and diagnostic point of view. Results of the non-invasive tests currently available make invasive tests unnecessary in the preoperative guidelines for these patients.     

An unusual cause of apparent regional hyperperfusion on radionuclide cerebral angiography study: case report

An unusual pattern of radioactivity in the venous phase was noted in the 99mTc-DTPA cerebral angiogram of a patient with persistent headaches. Initially the possibility of a small arteriovenous malformation with large draining veins was considered. However, contrast angiography revealed dilated cerebral veins with significant arteriovenous shunting. The differential diagnosis of regional hyperperfusion on the radioactivity study is discussed.     

The placebo in modern medicine

PURPOSE: To report the results of balloon angioplasty in recurrent carotid occlusive disease and evaluate the potential for stent implantation. METHODS AND RESULTS: Between April 1991 and September 1995, 15 patients with carotid restenosis underwent 17 endoluminal procedures in 3 common carotid and 14 internal carotid arteries. Two postdilation complications (dissection and acute occlusion) required prompt stenting; one common carotid artery was stented for postdilation residual stenosis. One recurrent lesion was also stented 6 months after initial angioplasty. One stroke, 1 silent cerebral infarction, and 3 transient ischemic attacks occurred in the balloon angioplasty patients (33% neurological complication rate). The common carotid stent patient died 3 days postoperatively due to hyperperfusion syndrome. Long-term follow-up in two stent patients showed no restenosis at 18 and 48 months, respectively. The 11 balloon angioplasty patients likewise have not demonstrated restenosis. CONCLUSIONS: Balloon angioplasty alone appears too risky for treating recurrent carotid disease. Stents may offer a safer alternative, particularly when implanted primarily.     

Flow and compartmental weight in relation to the cours of stroke

Using a scintillation camera system, hemispheric and regional cerebral blood flow was measured repeatedly during the course after a stroke. In 20 patients who improved clinically mean hemispheric and regional flow and relative weight of rapidly perfused compartment increased, while these values decreased in 15 patients, on an average, whose clinical condition deteriorated or did not change. The changes of flow and relative weight were significantly different between the two groups. Futhermore, the relationship between changes in clinical condition, scored according to a rating scale, and changes in flow and compartmental weight was proved by significant Spearman rank correlation coefficients. In six cases hyperperfused areas in locations of disturbed neurological function were observed; these areas were found to be ischemic at measurements done early and late in the cours after the stroke. This type of hyperperfusion was related to beneficial prognosis. The results indicate a shift of tissue form fast to slowly cleared compartment after a cerebrovascular attack. If tissue morphology is not entirely destroyed, recovery might occur; this results in an increase of recorded weight of rapidly clearing compartments, which correlates to the clinical course.     

Cerebral infarction associated with nephrotic syndrome in a young adult: a case report

We report a 19-year-old man who developed a cerebral infarction in the territory of the anterior choroidal artery and showed a hypercoagulable state and nephrotic syndrome after diarrhea and appetite loss. He had suffered from nephrotic syndrome from the age of three and had been treated for five years. MR-angiography showed an occlusion originating in the right internal carotid artery. The right anterior and middle cerebral arteries were imaged from the left internal carotid artery via the anterior communication artery. He showed symptoms of left hemiparesis, agnosia, loss of activity, anasarca and left hypacusis following his clinical course, but had recovered from all but left hemiparesis following medical treatments including steroid therapy. The histologic finding by a renal biopsy revealed focal glomerulosclerosis. In this case, we considered that when he was in a hypercoagulable state and had a second attack of nephrotic syndrome because of inflammation and dehydration due to diarrhea and appetite loss, his hypercoagulable state grew worse, and he then developed a cerebral infarction. When one see a patient with nephrotic syndrome, one should be attentive to the possibility of a complication of cerebral infarction.     

Regional cerebral blood flow during and after 2 hours of middle cerebral artery occlusion in the rat

In this study we explored if the secondary bioenergetic failure, which occurs a few hours after recirculation, following transient middle cerebral artery occlusion (MCAO) in rats, is caused by a compromised reflow. We induced 2 hours of MCAO and measured CBF at the end of the ischemia, as well as 15 minutes, 1, 2, and 4 hours after the start of recirculation, using autoradiographic or tissue sampling 14C-iodoantipyrine techniques. After 2 hours of MCAO, the autoradiographically measured CBF in the ischemic core areas was reduced to 3 to 5% of contralateral values. The reduction in CBF was less in neighboring, penumbral areas. After recirculation, flow already normalized in core tissues after 15 minutes, and remained close to normal for the 4 hours recirculation period studied. However, in penumbral tissues, recovery CBF values were usually below normal. The results show that tissues that are heavily compromised by the 2-hour period of ischemia and are destined to incur infarction, show a "relative hyperemia" during recirculation. In fact, some areas of the previously densely ischemic tissue showed overt hyperperfusion. This finding raises the question whether the relative or absolute hyperemia reflects events that are pathogenetically important. Because drugs that clearly ameliorate the final damage incurred fail to alter the relative hyperperfusion of previously ischemic tissues, it is concluded that vascular events in the reperfusion period do not play a major role in causing the final damage.     

The influence of socioeconomic and nutritional status on menarche in Nigerian school girls

Two once-daily electroconvulsive shocks (ECS) produced retrograde amnesia in rats trained on a Hebb-Williams maze; Verapamil (12.5 mg/kg, i.p.) or felodipine (10 mg/kg, p.o.) administered half an hour before each ECS attenuated this ECS-induced amnesia. Hence, these drugs may hold promise for the containment of amnesia induced by electroconvulsive therapy (ECT). Speculatively, one or more of several mechanisms may be involved: cerebral vasodilatation, enhancement of cholinergic tone, and inhibition of calcium-mediated impairment of neuronal function. These drugs may also act by attenuating the systolic surge in blood pressure during ECT, thereby decreasing edema due to cerebral hyperperfusion, as well as decreasing the possible transfer of potentially neurotoxic macromolecules through a putative breach in the blood-brain barrier.     

Optimized method for the determination of organophosphorus pesticides in meat and fatty matrices

A female patient with an ischaemic focal lesion in the non-dominant cerebral hemisphere due to stenosis of the right carotid artery is presented. Besides a mild left hemiparesis the clinical symptomatology included a pronounced hemi-neglect syndrome in the form of unilateral limb akinesia, a failure to respond to stimuli presented to the left of the midline as well as anosognosia and anosodiaphoria. Despite the 6-week rehabilitation training, the neglect syndrome was rather stabilized with only a slight tendency for improvement.     

Postischemic application of lipid peroxidation inhibitor U-101033E reduces neuronal damage after global cerebral ischemia in rats

BACKGROUND AND PURPOSE: The lipid peroxidation inhibitor U-101033E was examined for effects on cerebral blood flow (CBF), cortical tissue hemoglobin oxygen saturation (HbSo2), and neuronal damage. METHODS: Fifteen minutes of global cerebral ischemia was induced by two-vessel occlusion and hypobaric hypotension. Wistar rats (n = 25) were randomized to receive vehicle (n = 9) or 40 mg/kg U-101033E (n = 9) intraperitoneally during 2 hours of reperfusion. A sham group (n = 7) had neither ischemia nor therapy. Histology was evaluated 7 days after ischemia. RESULTS: During late hyperperfusion (at 17 minutes), vehicle-treated animals had a higher (P = 0.044) cortical tissue HbSo2 (72.0 +/- 1.4%) than did U-101033E-treated animals (65.8 +/- 2.5%). Neuronal counts in the superficial cortex layer found after 7 days correlated negatively with rCBF (r = -0.76; P < 0.001) or cortical tissue HbSo2 (r = -0.56; P = 0.028) assessed during the late hyperperfusion phase. U-101033E reduced neuronal damage in hippocampal CA1 from 64.3 +/- 9.2% to 31.2 +/- 8.4% (P = 0.020), as well as in the superficial cortical layer from 53.5 +/- 14.6% to 12.8 +/- 11.7% (P = 0.046). While animals in the vehicle group had reduced counts in all four examined cortex layers (P < 0.05 versus sham group), there was significant cortical neuron loss in the U-101033E group in only one of four areas. U-101033E had no effect on resting CBF or CO2 reactivity. CONCLUSIONS: Postischemic application of U-101033E protects hippocampal CA1 and cortical neurons after 15 minutes of global cerebral ischemia. The results indicate that free radical-induced lipid peroxidation contributes to reperfusion injury, a process that can be inhibited by antioxidants such as U-101033E.     

High prevalence of bihemispheric structural and functional defects in Sturge-Weber syndrome

Abnormal cerebral venous drainage is associated with hypoxia and glucose deprivation, which can account for progressive neurologic deterioration in Sturge-Weber syndrome. Although developmental delay is common in Sturge-Weber syndrome, bihemispheric calcification is uncommon. Computed tomography (CT) and magnetic resonance imaging (MRI) were used to study the neuroanatomy, while single photon emission computed tomography (SPECT) was used concurrently to evaluate perfusion and glucose metabolism using 99mTc hexamethylpropyleneamine oxime (HMPAO) and [18F] fluorodeoxyglucose (FDG), respectively. Ten patients (10 to 22 years of age) with previously diagnosed Sturge-Weber syndrome, port-wine nevi, and clinical evidence of seizures or stroke-like episodes were studied. Five children with onset of seizures in the first year of life had overall clinical severity comparable to that of children with later-onset seizures. Calcification was present in both hemispheres in one patient; six additional patients had other radiologic evidence of bihemispheric disease; SPECT studies detected bihemispheric disease in four cases. Our study is the first to concurrently evaluate structure, perfusion, and glucose metabolism in Sturge-Weber syndrome and to show a mismatch between functional and structural brain imaging in both cerebral hemispheres. Widespread abnormalities of cerebral perfusion and glucose metabolism might explain the high prevalence of developmental delay associated with Sturge-Weber syndrome. Longitudinal studies are needed to define better the natural history of neurologic deterioration and radiologic progression that relates to central nervous system circulatory dysfunction in Sturge-Weber syndrome.     

Cerebral fat embolism studied by magnetic resonance imaging, transcranial Doppler sonography, and single photon emission computed tomography: case report

Cerebral fat embolism syndrome is an uncommon complication of trauma. We present a patient who developed cerebral fat embolism syndrome secondary to long-bone fractures. Although computed tomography of the brain failed to show any intracranial lesion, magnetic resonance imaging (MRI) detected scattered, high-signal-intensity lesions on T2-weighted images. 99mTc-d, 1-hexamethyl-propylene amine oxine single photon emission computed tomography (99mTc-HMPAO SPECT) and transcranial Doppler sonography (TCD) demonstrated low cerebral blood flow in the acute stage. MRI, 99mTc-HMPAO SPECT, and TCD correlated well with the clinical course of cerebral fat embolism syndrome.     

Genetic markers in the blood of animals: a historical review

One-photon emission computed tomography (OPECT) was used to examine 87 patients with the epileptiform syndrome. Eighty five patients had impaired drug distribution which was suggestive of varying degree cerebral circulatory disorders. OPECT with a Tc-99m-gm-pao used in patients with the epileptiform syndrome revealed the morphological substract of brain structures. OPECT findings in the patients suggested the brain structural microcirculatory changes to be diffuse and focal, of varying magnitude. There was no clear correlation between clinical manifestations and OPECT and CT findings.     

N-3 and n-6 fatty acid metabolism in undifferentiated and differentiated human intestine cell line (Caco-2)

Antiphospholipid antibody is associated with a clinical syndrome of vascular thrombosis, thrombocytopenia, recurrent fetal loss and livedo reticularis, whether or not a clinical diagnosis of systemic lupus erythematosus (SLE) coexists. Central nervous system involvement in SLE is multifactorial, thrombotic events, antineuronal antibodies, hypertension, infection, side effects of drugs etc. Antiphospholipid antibodies may play a role in focal neurological manifestations in SLE. In the absence of SLE, different neurological symptoms are well associated with antiphospholipid antibodies including stroke, seizures, dementia, migraine, ocular ischemia, chorea, transverse myelopathy, cerebral phlebitis. Other association are more controversal like Guillain Barré syndrome, motor neuron disease, communicating hydrocephalus. In all patients with antiphospholipid antibodies with neurological involvement, cerebral MRI may be performed with an echocardiographic study because a possible association with Libman and Sacks endocarditis, valve dysfunction or cardiac thrombus source of cerebral ischemia.     

Failures, problems and hopes in the transformation of health services. I. Causes of erroneous decisions in the beginning phases of transformation

Vascular damage is a well known cause of hypopituitarism since Sheehan's report of postpartum pituitary necrosis; it has subsequently been reported that also sickle-cell anemia, eclampsia, pituitary apoplexy and other pathologies may induce failure of the anterior hypophysis through this mechanism. The antiphospholipid syndrome (APS) is characterized by widespread arterial and venous thrombosis with resulting different clinical features; Addison's disease due to adrenal thrombosis is the only endocrine involvement reported so far in this syndrome. We report here a case of global anterior pituitary insufficiency which developed soon after cerebral ischaemic stroke in a 62 year aged woman with Lupus aicoagulant activity (LAC) and large atrial thrombosis; underlying pathologies were excluded by appropriate investigations. Therefore in our opinion this is the first case in which anterior hypopituitarism is reported in the clinical constellation of APS and the second type of endocline involvement.