Subarachnoid neurocysticercosis with occlusion of the major intracranial arteries: case report

Cysticercosis is the most common parasitic disease affecting the central nervous system. Stroke is a recognized complication of neurocysticercosis, occurring in 2 to 12% of cases, mostly in the form of small lacunar infarcts. We report a case of hemiparesis and aphasia in a 51-year-old Hispanic woman, which was secondary to complete occlusion of the left internal carotid and bilateral anterior cerebral arteries. Magnetic resonance imaging demonstrated the presence of enhancing subarachnoid material surrounding these occluded cerebral arteries, providing antemortem, noninvasive documentation of the inflammatory meningeal cysticercotic reaction that was presumably responsible for the occlusive arteritis causing the cerebral infarction. This represents the third reported case of internal carotid artery occlusion and the first reported case of anterior cerebral artery occlusion secondary to neurocysticercosis.     

Agenesis of internal carotid artery associated with aneurysm of anterior communicating artery (author's transl)

A case of agenesis of the left internal carotid artery with an aneurysm of the anterior communicating artery was reported in detail. The patient was a 48-year-old man who had an episode of subarachnoid hemorrhage about 10 years ago. This time left heminumbness and motor weakness of the left lower extremity occured and he was brought our hospital. Right common carotid angiography, left retrograde brachial serial angiography and aortography demonstrated an agenesis of the left internal carotid artery, an aneurysm of the anterior communicating artery, tortuous megadolic hobasilar artery and anomalies on the circle of Willis such as absence of supra optic portion of the right anterior cerebral artery, and large left posterior communicating artery. We confirmed latter findings by operation. After successful neck clipping of the aneurysm, his clinical findings were remarkably improved.     

Refusion of anterior cerebral artery after aneurysm clipping--a case report

Herein, we are describing an unusual case suffering from a left anterior cerebral artery aneurysm (A1). Both the anterior cerebral arteries were supplied by the left internal carotid artery as was found in digital substraction angiography (DSA) preoperatively. The postoperative angiograms revealed that left anterior cerebral artery was supplied from the left internal carotid artery and the right anterior cerebral artery by the right internal carotid artery respectively. This finding of cerebral angiograms is interesting and rarely mentioned in the literature. Its hemodynamic change and pathogenesis were unclear and different to that of the coronary circulation, ischemic change of gut and skeletal muscle. The causes may include: 1) vasospasm at the anterior communicating artery after manipulation at surgery; 2) desiccation or shrivelling the adjacent artery by intraoperative electrocoagulation; 3) occlusion the anterior communicating artery by the wing of clip. 4) the deprivation of the blood flow from the left internal carotid artery after totally or partially narrowing left A1 by an aneurysm clip. The redistribution of blood volume in the previously hypoplastic right anterior cerebral artery and decreased caliber of the left anterior cerebral artery (A1) are likely playing a role in this case.     

Massive infarcts involving the territory of the anterior choroidal artery and cardioembolism

BACKGROUND AND PURPOSE: At neuropathological examination, the territory of the anterior choroidal artery is frequently found to be involved in massive infarcts of the internal carotid artery territory. The aim of our study was to analyze the clinical spectrum, the course, and the mechanism of these massive infarcts compared with the rare infarcts involving only the anterior choroidal artery territory. METHODS: Retrospective clinical examination and pathological study were performed in 35 patients with cerebral infarcts affecting at least the territory of the anterior choroidal artery. RESULTS: In no patient had the involvement of the anterior choroidal territory infarcts been recognized clinically, nor had the triad of clinical signs (hemiplegia, hemianesthesia, and hemianopsia) classically seen in infarcts restricted to this territory been found alone. Impairment of consciousness, cognitive disorders, or oculomotor palsies had been found in addition to one or more signs of the triad. This was probably related to the involvement of other territories (94%), especially the middle cerebral artery territory (68%) and the posterior cerebral artery territory (20%). The concomitant involvement of several territories was due most frequently to an occlusion of the internal carotid artery, which was found at autopsy in 74% of the patients. These occlusions were often associated with cardioembolism (54%). In contrast, artery-to-artery embolism (17%) and small-artery disease (6%) were seldom found. Only two cases of infarcts restricted to the anterior choroidal artery territory were observed. CONCLUSIONS: The involvement of the territory of the anterior choroidal artery in massive infarcts was due mainly to a cardioembolic occlusion of the internal carotid artery.     

Combined intraoperative retrograde stent implantation and thrombendarterectomy of the carotid artery

HISTORY AND CLINICAL FINDINGS: A 63-year-old man developed recurrent transitory ischaemic episodes of vertigo and weakness in the legs 6 weeks before admission. 3 weeks later he had a left amaurosis fugax. A stenotic murmur was heard over the left carotid artery. INVESTIGATION: Intraarterial digital subtraction angiography of the arteries to the head revealed occlusion of the right internal carotid artery (RICA) and marked narrowing at the origin of the left common carotid artery (LCCA), which could not be passed by catheter. TREATMENT AND COURSE: As a catheter could not be passed into the LCCA, a stent was at operation placed retrogradely into it. Intraoperative angiography showed subtotal stenosis of the left ICA, which was treated by thrombendarterectomy and dacron patch-plasty. The postoperative course was without complication and the patient was free of symptoms. Follow-up angiography was unremarkable. CONCLUSION: If a stenosis of the carotid artery cannot be passed by catheter, intraoperative retrograde placement of a stent is an alternative to percutaneous antegrade transluminal angioplasty or surgical bypass.     

Differential diagnosis in dementia

The results of an autopsy of a 78-year-old female patient with an occluded of the right internal carotid artery after a traffic accident are reported. She presented with consciousness disturbance, right conjugate deviation, left hemiparesis and left pathological reflex. Evidence of right skull and clavicular fractures seemed to suggest that severe hyperextension of her neck associated with contralateral lateral flexion had stretched her carotid artery. Although she was treated with antiplatelet therapy, her cerebral swelling due to right global infarction progressed and she died due to bilateral cerebral herniation three days after injury. The autopsy disclosed right dissecting carotid artery occlusion and subadventitial dissection was revealed histologically. When a hematoma dissect the media and adventitia of the carotid artery wall, the outer wall weakens and may dilate without narrowing the lumen of the carotid artery. In this case, the vessel occlusion was considered to be due to a primary intramural hematoma which developed and subsequently ruptured through the intima into the vessel lumen. Early diagnosis and treatment are necessary for improving the prognosis of this disease entity. A patient with poor colateral flow, such as in this case, will show a rapid progression of cerebral infarction. It is best to consider surgical treatment in this case if the other traumatic lesions are able to tolerate surgery.     

Pulmonary tuberculosis revealed by lupus vulgaris in an immunocompetent patient

In patients with severe carotid stenosis or total occlusion, episodic contralateral motor dysfunction is more likely related to cerebral hypoperfusion than epileptogenic activity. A man with orthostatic-mediated right-sided limb shaking was found to have total left internal carotid artery occlusion. There was prominent reduction of cerebrovascular reserve seen on single photon emission computed tomography (SPECT) performed with and without acetazolomide. During assumption of an upright position transcranial Doppler (TCD) revealed a marked attenuation of the left middle cerebral artery flow pattern not associated with changes during electroencephalographic monitoring, even after administration of acetazolomide. In this man, limb shaking episodes were attributed to hypoperfusion of the contralateral cerebral hemisphere, and not to epileptogenic activity.     

Paradoxical cerebral embolism during fibrinolysis therapy in deep vein thrombosis and pulmonary embolism

A 37-year-old woman with increasing dyspnoea over several months suddenly developed severe ortho- and tachypnoea as well as cyanosis of the lips and acrocyanosis. Pulmonary angiography revealed massive bilateral pulmonary emboli with a systolic pulmonary artery pressure of 75 mm Hg. Phlebography demonstrated a thrombotic occlusion of the deep veins of the left leg extending to the distal femoral vein. Thrombolysis treatment was started via an indwelling pulmonary artery catheter (500,000 IU urokinase and 10,000 IU heparin as bolus, then 1 mill. IU urokinase and 1,000 IU heparin per hour). After two hours an incomplete left-sided paresis occurred (involving ocular and facial muscles, dysarthria, left arm and left leg) and the thrombolytic infusion was stopped. But cerebral computed tomography (CT) did not demonstrate any intracerebral haemorrhage. The heparin infusion was restarted (partial thromboplastin time between 70 and 90 s). CT examinations during the next few days showed the development of an ischaemic infarction in the distribution of the right medial cerebral artery. Angiography demonstrated occlusion of the right internal carotid artery. The diagnosis of a paradoxical embolus was supported by easy cardiac catheter passage through a patent foramen ovale. Subsequent pulmonary angiography demonstrated a thrombus-free pulmonary arterial circulation with a normal pulmonary arterial pressure. There was gradual and extensive regression of the incomplete hemiparesis.     

Internal carotid artery occlusion related to seat belt shoulder strap: report of two cases

Two cases of traumatic internal carotid artery occlusion probably related to the seat belt shoulder strap are reported. Case 1. A 20-year-old woman was driving and was struck on the right front side of her car by another car. There were neither bruises, abrasions on her neck, nor weakness in her extremities. About 4 hours later, she developed left hemiplegia, and CT scan taken on the following day revealed low density areas in the capsulostriatal area on the right. The right carotid angiography revealed occlusion of the internal carotid artery about 3 cm distal to the bifurcation. Case 2. A 43-year-old man was driving and was struck on the front of his car by a hard iron railing. He sustained a sternum fracture, but there was no disturbance of consciousness or paresis of the extremities. His neck was unremarkable externally. About 50 days later, he developed left hemiplegia. CT scan and MRI revealed a massive infarction in the distribution of the right middle cerebral artery territories. The carotid angiography revealed occlusion of the right internal carotid artery about 3 cm distal to the bifurcation. In each cases, the driver was wearing a three-point shoulder seatbelt when the car was struck on the front or on the right front. Previous experimental studies have revealed in these situations the neck is flexed right anteriorly, and then quickly overextended left posteriorly. The overextension of the neck probably injured the intima of the internal carotid artery ipsilateral to the shoulder fixed in the seatbelt, resulting in the subsequent occlusion by a thrombus.     

A case of multiple cerebral arterial thrombosis due to congenital protein C deficiency]

We report a 49-year-old man who had right hemiparesis and motor aphasia. A computed tomography revealed hypodense areas in the left frontal subcortex. A cerebral angiography demonstrated occlusion of the left distal internal carotid artery and both anterior cerebral arteries, as well as stenosis of the left internal carotid artery at the cervical portion. The second angiogram obtained a month later showed no changes. The diagnosis of atherothrombotic cerebral infarction was established on the basis of clinical profile and angiographic findings. Protein C activity and antigen levels were reduced to approximately one half of the normal level in the patient and his brother. The patient had no other risk factors for stroke. Protein C deficiency has been considered one of the risk factors for thrombotic diseases. Venous thrombosis is the most common clinical manifestation, whereas arterial thrombosis is relatively rare. It is generally believed that arterial ischemic stroke associated with protein C deficiency occurs with embolic mechanism, and atherothrombotic infarction is extremely rare. This is the first report suggesting the possibility that protein C deficiency can cause cerebral thrombosis.     

Photodynamic therapy for early stage squamous cell carcinoma of the lung

We studied 9 patients with bilateral vertebral artery occlusion (BVAO). BVAO was confirmed using angiography in order to clarify its clinical feature, mechanism, and long term prognosis. Three patients showed bilateral intra-cranial occlusion, 3 bilateral extra-cranial occlusion, and 3 intra and extra-cranial occlusion. The basilar artery was fed by the posterior communicating artery in 8 out of 9 patients. In one of the 8, reconstitution of the thyrocervical artery was seen. We divided the patients into 4 groups according to MRI findings, as follows: Group 1 with no abnormal finding on MRI (N = 2); Group 2 with deep pontine infarcts and non-territorial small cerebellar infarcts (N = 2); Group 3 with extended pontine infarcts (N = 3); and Group 4 with cerebellar cortical artery infarcts, deep pontine infarcts, and non-territorial small cerebellar infarcts (N = 2). Transient episodes were seen in all patients, 8 patients out of 9 had vertigo/dizziness, 3 tinnitus, 2 diplopia, 2 headache, 2 numbness, and 1 hearing disturbance. These episodes preceded a final attack or complete stroke 2 days to 5 months, and those who had a longer period of episodes in the preceding term tended to have less severe deficits. Six of the patients had vertebro-basiler symptoms after being in the upright position, including all the patients in Groups 2 and 4, which had cerebellar border zone/terminal zone infarcts. These results indicate that the hemodynamic mechanism plays an important role in BVAO. The prognosis was not always grave. Four of the patients could walk independently, 2 could walk with a cane, and 3 were bed ridden (2 of which died). Long-term follow-up data (a mean of 5 years) were obtained in all patients. In the patients who could walk, one had asymptomatic cerebellar infarcts, and one had TIAs frequently. Patients with BVAO often also have TIAs and/or preceding episode and show cerebellar border zone/terminal zone infarcts. This research strongly suggests that hemodynamic mechanism might play an important role in BVAO, and that paying attention to border zone infarction in MRI and transient episodes can lead to earlier diagnosis and treatment.     

Collateralization of an occluded internal carotid artery via a vas vasorum

BACKGROUND: Reopening of an occluded internal carotid artery (ICA) is often seen in dissections but only rarely occurs in atherothrombotic occlusion of the internal carotid artery. CASE DESCRIPTION: A 60-year-old man suffered a minor stroke with dysphasia in March 1995. Color-coded duplex ultrasonography of his neck arteries revealed a left ICA occlusion. He was placed on a regimen of aspirin and followed up clinically and with ultrasonography. At follow-up 18 months later, the patient was asymptomatic. On duplex ultrasonography his left occluded ICA was found to be reopened, with a residual, proximal, high-grade stenosis. However, intra-arterial digital subtraction angiography demonstrated a persistent ICA occlusion and a vas vasorum originating from the carotid bulb and draining into the ICA distal to the occlusion. CONCLUSIONS: The rare collateralization of an occluded ICA by vasa vasorum seems to take several months. It can be a pitfall in the ultrasound diagnosis of carotid artery occlusive disease.     

Testosterone sulphation and glucuronidation in the human liver: interindividual variability

We present a case with the traumatic extracranial internal carotid artery dissecting aneurysm. A 21-year-old man was involved in a motorcycle accident, resulting in multiple injuries but no apparent head and neck injuries. Head CT was normal on his admission. He was discharged from his local hospital 3 weeks after the accident without any neurological deficits. Five weeks after the accident, he suddenly presented with a motor aphasia and a right hemiparesis. CT and MRI showed infarctions in the left para-Sylvian and the left angular areas. Angiography showed a left extracranial carotid artery dissecting aneurysm at the level of C1 vertebral arch. The patient was initially managed by an anticoagulant agent, but he suffered from another transient ischemic attack due to distal embolism from the aneurysm. Balloon occlusion test of the left ICA was performed under monitoring EEG, SEP. Mean stump pressure (MSP) revealed 60 mmHg. and MSP/Mean systematic blood pressure revealed 67%. We judged that the left ICA ligation was a safe method to treat this patient, however, considering the patient's age and the side of the lesion, left STA-MICA bypass and ligation of the left ICA were carried out in one stage. Postoperatively, the patient did not show any cerebral ischemic complications and angiography showed disappearance of the aneurysm and patency of the bypass. The left MCA territories were filled well by cross circulation and the bypass.     

Progressive intracranial occlusive disease associated with deficiency of protein S. Report of two cases

BACKGROUND AND PURPOSE: Deficiency of the free fraction of protein S has been associated with arterial or venous stroke. The pathogenesis of vascular occlusion in patients with protein S deficiency is not known. We present two cases of cerebral infarction and deficiency of protein S in which the subjects had progressive intracranial occlusions. CASE DESCRIPTION: A 16-year-old girl was admitted because of left brain stem infarction and protein S deficiency. Cerebral angiography disclosed stenosis of the right intracranial vertebral artery and occlusion of the left posterior cerebral artery. A second angiogram performed 18 months later disclosed occlusion of the right vertebral intracranial artery. In the second case, a 17-year-old girl was admitted because of left hemispheric cerebral infarction and protein S deficiency. Cerebral angiography showed stenosis of the left anterior cerebral artery, left supraclinoid internal artery, and left middle cerebral artery. A second cerebral angiogram performed 5 months later disclosed occlusion of the left anterior cerebral artery and poor hemispheric perfusion through the left middle cerebral artery. CONCLUSIONS: Based on our cases, we postulate that some patients with prothrombotic states may develop progressive intracranial arterial occlusions, possibly secondary to a permanent thrombogenic stimulus. We suggest routinely searching for prothrombotic states in young patients with intracranial occlusion, especially if the occlusion is progressive and other causes are not obvious.     

Ischaemic stroke from cerebral embolism in cephalic fibromuscular dysplasia

Fibromuscular dysplasia (FMD) of the internal carotid arteries and its relationship with focal cerebral ischaemia is unproven. This vasculopathy is often detected incidentally during a cerebral angiogram for non-ischaemic cerebral events. FMD affects the proximal one-third of the internal carotid artery in almost all cases and is bilateral in 60% to 85%, with middle-aged women affected in 85% of the cases. Ischaemic stroke has been postulated to result from severe stenosis or thrombotic occlusion at the FMD site. Cerebral embolism from FMD has rarely been reported. We report 3 young patients with acute ischaemic stroke who had FMD on cerebral angiography. They presented with a focal hemispheric stroke where the probable pathophysiology is embolism to the distal internal carotid artery from thrombus formed at the proximal FMD site. The patients were all males, with unilateral proximal internal carotid artery FMD lesions and occlusion of the internal carotid artery distally on the same side. All were extensively investigated and no other causes for stroke were found.     

Post-traumatic hemiplegia in a patient with fibromuscular dysplasia of the carotid artery

A 44-year-old patient, without remarkable medical history, was admitted with a head trauma with initial loss of consciousness and a thoracic trauma. The initial treatment included the insertion of a chest drain for evacuation of a pneumothorax and intrapleural analgesia with bupivacaine. The day after admission, the patient experienced a generalized epileptic crisis, without prodomes. Later, a left proportional hemiplegia with aphasia was recognized. The CT scan obtained immediately after the crisis, as well as the carotid Doppler ultrasonography and echocardiography were normal. The bilateral carotid angiography showed an image of fibromuscular dysplasia of the extracranial segment of the right internal carotid artery. The migration of a carotid thrombus initiated by the trauma was hypothetized. A treatment with a platelet aggregation inhibiting drug was started and associated 20 days later with low molecular weight heparin. The patient recovered a normal motility within 10 days; only the aphasia remained. Trauma of the carotid artery is not a frequent cause of cerebrovascular accident. The occurrence of the latter is favoured by a pre-existing lesion of this artery. This case demonstrates that in a trauma patient not all central nervous system manifestations are initiated by a head trauma.     

MR demonstration of a giant cavernous carotid aneurysm with occlusion of the contralateral intracranial carotid artery: an unusual complication of cavernous sinus thrombosis

We present an unusual combination of vascular complications of cavernous sinus thrombosis in a 7-year-old girl. MRI and MR angiography showed occlusion of the intracranial portion of the left internal carotid artery and a contralateral giant cavernous carotid aneurysm. This combination of vascular findings may influence the management in such cases.     

Thrombolytic therapy in acute occlusion of the intracranial internal carotid artery bifurcation

PURPOSE: To evaluate efficacy and clinical benefit of early thrombolytic therapy in intracranial internal carotid artery occlusion. METHODS: Thirty-two patients (mean age, 56 years) with acute intracranial internal carotid artery occlusion were studied clinically and with CT and angiography before and after thrombolytic therapy with intravenous alteplase (n = 16), superselective intraarterial alteplase (n = 8), and superselective intraarterial urokinase (n = 8). RESULTS: Initial CT showed a large parenchymal hypodensity in 11 (34%) patients, a small hypodensity in 15 (47%) patients, and no hypodensity in 6 (19%) patients. Recanalization after thrombolytic therapy was observed in 4 patients (12.5% in each treatment group). Follow-up CT showed six hemorrhagic infarcts and four parenchymal hematomas unrelated to recanalization, alteplase, or urokinase administration, but commonly associated with intraarterial treatment. Clinical outcome was fatal in 53%, poor in 31%, and moderate or good in 16% of the patients. Outcome was equal in different treatment groups and closely linked to both the quality of leptomeningeal collaterals and the extent of parenchymal hypodensity on the first CT. CONCLUSION: Because intravenous or intraarterial treatment with alteplase or urokinase fails to recanalize the vascular obstruction, it does not improve the prognosis of intracranial internal carotid artery occlusion over that of the natural course. Improved results may be possible with novel recanalization techniques.     

Color Doppler echography in the study of pseudo-occlusion of the internal carotid

The differentiation of pseudo-occlusion from complete internal carotid artery occlusion may have important clinical consequences for patients with the former tend not to benefit from reconstructive surgery. The Authors report a case in which color-Doppler duplex-scanner revealed a persisting string-like lumen that was not demonstrated by angiography. The Authors believe that ultrasonography may in future permit the reliable differentiation of pseudo-from complete carotid occlusion, thereby reducing the need for angiography.     

Computed tomographic angiography for the evaluation of carotid artery stenosis

BACKGROUND AND PURPOSE: No previous study has compared the reliability of carotid artery measurement provided by axial images, shaded surface display (SSD), and maximum intensity projection (MIP). METHODS: Helical CT and conventional angiography were performed prospectively in 20 patients with atherosclerotic stenosis of the internal carotid artery. Stenosis measurement was performed in a blinded fashion on angiography and CT by two independent examiners. Calcifications were segmented when they were located far enough from the vascular lumen. SSD and MIP were systematically performed for each carotid bifurcation. We measured stenosis using conventional angiography as standard and the different CT reconstructions (axial images, SSD, and MIP) by comparing the stenosis diameter at its narrowest point to the normal internal carotid artery. The degree of stenosis was classified into six groups: no stenosis, mild stenosis (< 30%), moderate stenosis (30% to 70%), severe stenosis (> 70%), near occlusion, and occlusion (100%). No measurement was made in cases of normal artery, near occlusion, and occlusion. RESULTS: Correlations between angiography and the three types of reconstruction were very good. Axial sections correctly classified the carotid arteries in 95% of cases. In 10 carotid arteries, stenosis was not assessable by SSD and MIP because of calcifications. In the remaining carotid arteries, MIP correctly classified the degree of stenosis in 96% of cases, whereas SSD misclassified 21% of cases. CONCLUSIONS: Our study showed that axial images provide a reliable evaluation of carotid artery stenosis. Calcifications are limiting factors in SSD or MIP. When atherosclerotic plaques are not calcified, MIP reconstructions provide a more reliable measurement of the vascular lumen than SSD.