A case of juvenile cerebral infarction caused by bilateral anterior cerebral artery dissection]

A 38-year-old man was admitted to our hospital with headache, dysarthria and paraparesis. Brain CT and diffusion MRI disclosed cerebral infarction at bilateral anterior cerebral artery (ACA) territories. His symptoms and signs deteriorated in several days despite intensive antithrombotic therapy, resulting in right hemiparesis, akinetic mutism, memory disturbance, change of personality, urinary incontinence, forced grasping, and starting delay of speech and motion. Cerebral angiography demonstrated occlusion with contrast pooling at the right ACA A2 portion. Stenosis and dilatation were found at left ACA A2 portion. An intimal flap was also demonstrated on serial angiography. This case was diagnosed as cerebral infarction caused by dissection of bilateral ACA. Although no definite primary arteriopathy was demonstrated, bilateral dissection could be occurred simultaneously.     

A case of subarachnoid hemorrhage verified as cerebral vasospasm by using three-dimensional CT angiography (3 D-CTA): reference to comparison with conventional angiography]

The authors present a case of aneurysmal subarachnoid hemorrhage that were verified as cerebral vasospasm by using both three-dimensional CT angioraphy (3 D-CTA) and conventional angiography. A 45-year-old man was referred to our department 4th day after sudden onset of a severe headache. On admission, emergency 3 D-CTA showed the cerebral vasospasm involving M 1 segment. Conventional angiography performed at the same day of the left internal carotid artery confirmed the cerebral vasospasm of the same vessel as 3 D-CTA, and furthermore demonstrated the left middle cerebral artery (MCA) and anterior cerebral artery (ACA) genu aneurysms. The former was seen as a ruptured aneurysm from brain CT findings (Fisher group 3). On the 10th day after the onset, 3 D-CTA demonstrated the remaining severe cerebral vasospasm of the supraclinoid portion of left ICA and M 1 segment. Findings at the conventional angiography subsequently performed were concordant with those of 3 D-CTA. The patient was successfully treated with delayed surgical clipping for both aneurysms without the symptoms related to the cerebral vasospasm and discharged without neurological abnormality. We consider that 3 D-CTA shows promise as a minimally invasive method of evaluating the cerebral vasospasm and would take the place of the conventional angiography.     

A case of anterior cerebral artery dissection causing hemorrhagic infarction]

A 56-year-old man presented with weakness in his right arm and leg. Throbbing headache occurred several hours prior to his weakness. Brain CT obtained on day 3 demonstrated low density areas in the medial part of the left frontal lobe. Cerebral angiography on day 14 demonstrated dilatation and narrowing of the left anterior cerebral artery (ACA) corresponding to "pearl and string sign". The diagnosis of spontaneous ACA dissection was established with clinical features, laboratory findings, and angiographic findings. Antiplatelet therapy was undertaken for the prevention of ischemic events. Serial Brain CT demonstrated hemorrhagic change in the area of infarction. However, there was no definite clinical deterioration. Antiplatelet therapy was withdrawn after hemorrhagic change was noted. Cerebral angiography on day 35 showed improvement of both dilatation and narrowing. Possible reperfusion injury caused by absorption of intramural hematoma seems to be responsible for hemorrhagic change. In patients with cerebral infarction due to dissection of intracranial arteries, antithrombotic therapy is controversial as hemorrhagic complications including hemorrhagic infarction as well as subarachnoidal hemorrhage can occur. Further accumulation of cases is required.     

Multiple cerebrovascular occlusive disease associated with neurofibromatosis

Multiple cerebrovascular occlusive disease is rarely seen in patients with neurofibromatosis. Two cases of such lesions are presented and literatures dealing with the clinical and angiographical aspects of this occlusive disease are reviewed. Case 1; A 38-year-old normotensive man had sudden onset of vomiting, left hemiparesis and disturbance of consciousness, one day before the admission. He had family history of neurofibromatosis, and examination showed café au lait spots over the body. CT scans revealed a subcortical hematoma in the right temporal lobe. Angiogram revealed multiple occlusive lesions of the cerebral arteries, including occlusions of the right internal carotid artery (ICA) at the distal end, middle (MCA) and anterior (ACA) cerebral artery at the proximal portion, and stenosis of the left ICA and ACA. Abnormal vascular networks at the base of the brain were also seen bilaterally. Decompressive craniectomy, removal of the hematoma and bilateral ventricular drainage were performed. Postoperative course was excellent. Angiogram performed five and a half years later, during which time without any surgical procedures, demonstrated no apparent angiographic differences from the previous one. Case 2; A 29-year-old woman without family history of neurofibromatosis presented with sudden onset left hemiparesis. Café au lait spots were found over the body. A CT scan revealed small infarctions in the territory of the right MCA, and angiogram demonstrated multiple occlusive lesions of the cerebral arteries, including stenosis of the bilateral ICA, the left MCA, both ACAs at the proximal portion, and the right posterior cerebral artery, and occlusions of the right MCA.(ABSTRACT TRUNCATED AT 250 WORDS)     

Two cases of cerebral embolism showing global aphasia without hemiparesis]

We report two cases of typical global aphasia without hemiparesis due to cerebral embolism. Case 1 was a 65-year-old right-handed man with a history of old myocardial infarction. No spontaneous speech was noted by his family. Neurological examination upon admission revealed confusional state, global aphasia, conjugate deviation to the left and slight drift of the outstretched right limbs. The right hemiparesis rapidly recovered after admission. CT scan performed on the second hospital day showed discrete low density areas in the left posterior frontal lobe and left temporo-parietal regions. The extent and severity of his global aphasia were unchanged. The second case was an 82-year-old right-handed man with a history of atrial fibrillation. He was admitted to our hospital one hour after he was found unable to speak. Neurological examination upon admission revealed global aphasia, conjugate deviation to the left and suspected right homonymous hemianopia by confrontation. There was no sign of hemiparesis. CT scan showed extensive low density area in the left temporo-parietal regions. In both cases, cerebral angiography failed to demonstrate any occlusion of intra- and extra-cranial blood vessels. IMP-SPECT showed a depression of cerebral blood flow in the left anterior and posterior watershed areas in case 1 and 2. In the literature, there have been 20 cases of global aphasia without hemiparesis including our two cases. In many cases, the initial symptom was inability or difficulty in speaking.(ABSTRACT TRUNCATED AT 250 WORDS)     

A case of intracerebral and subarachnoid hemorrhage of unknown origin with preceding headache]

We report a case of a 31-year-old female with multiple intracerebral hemorrhage and subarachnoid hemorrhage. She presented with headache one week before hemorrhage, and a CT scan performed at that time showed no abnormal findings. Neurological examination on admission revealed mild disturbance of consciousness, papilledema, and mild left hemiparesis. CT scans demonstrated intracerebral hemorrhage in the right caudate head and left frontal subcortex, and diffuse subarachnoid hemorrhage. Cerebral angiogram and laboratory examination revealed no abnormal findings. Erythrocyte sedimentation rate, C reactive protein and antiphospholipid antibody were within normal ranges. The patient underwent removal of hematoma by craniotomy. One week after the operation, a subcutaneous hematoma in the area of the craniotomy was found. Cerebral angiography demonstrated an aneurysm of the right superficial temporal artery, which was remote from the craniotomy. This aneurysm was surgically removed and examined. Histopathological examination revealed the presence of a pseudoaneurysm but no inflammation. Although primary angitis of the central nervous system was suspected to be the cause of this disease, a definite diagnosis could not be obtained.     

A rare case of subarachnoideal pneumocephalus after ear douche therapy

No detailed reports on pneumocephalus caused by any factors other than head trauma, and their courses accompanied with this disease have been so far available. We recently experienced a case of pneumocephalus complicated with severe clouding of consciousness, ocular deviation, and unilateral spatial neglect with the results being reported hereinafter. A 54-year-old man had often received ear douche therapy due to chronic sinusitis and tubal obstruction about 3 years before without any history of head trauma. On Jan. 6, 1984, sudden clouding of consciousness accompanying stiffness of the left arm occurred immediately after ear douche, and then he was transferred to our center. At admission, semicomatose, bilateral ocular deviation to the right, and left hemiparesis were observed. Plain skull X-ray films showed a retention of air in the frontal and temporal regions, while CT scan revealed air retention on the bilateral frontal region, bilateral temporal tip and suprasellar cistern. However, no abnormal findings were detected in the brain. Consciousness and hemiparesis recovered on the next day of hospitalization, however, the left hemispatial neglect still remained. This symptom was still observed on the 3rd day but disappeared by the 4th day of hospitalization. For clarifying its cause, cerebral angiography, CT scan and electroencephalography were then performed. CT scan revealed no anomalies in the brain, while cerebral angiography showed a cerebral circulation pattern in favor of the right internal carotid artery.(ABSTRACT TRUNCATED AT 250 WORDS)     

Anterior cerebral artery occlusion clinical analysis of 27 self-experienced cases

From the years 1977 through 1989, the author experienced 27 cases with only anterior cerebral artery (ACA) occlusion but without any other main cerebral arterial occlusions. These were proven by cerebral angiographies and verified by CT. Two patients showing large infarction in the left frontal lobe on CT but showing no evidence of arterial occlusion by cerebral angiography were also registered in this study because these patients were thought to have recanalized ACA. There were 15 males and 12 females with an age of 61.5 +/- 7.98 (mean +/- SD) and 66.1 +/- 6.45, respectively. Twenty two cases had cerebral thrombosis and 5 had cerebral embolism. There were 4 cases with bilateral ACA occlusions, 8 with right ACA occlusion and 15 with left ACA occlusion. Twenty two patients (81%) were alert on admission and this fact might explain their excellent ADL on discharge: full recovery in 9 patients (33%) and self-management in 12 patients (44%). Seventeen patients (63%) had a CT-proven infarcted area with a correlation to ACA occlusion (s), while 9 patients (33%) showed no correlation between an infarction on CT and an ACA occlusion. One patient showed no abnormal findings on CT. Four patients with right ACA occlusion were incidentally observed, even though their mode of onset was strokes. The symptoms of the other 23 patients were those of anterior cerebral artery syndromes: hemiparesis (74%), urinary incontinence (39%), forced grasping (39%), mutism (30%), indifference (26%) and apraxia (22%) etc.     

Persistent primitive first cervical intersegmental artery (proatlantal artery II) with occlusion of the basilar artery--a case report

A rare case of persistent primitive first cervical intersegmental artery (proatlantal artery II) is reported. A 58-year-old man was admitted to our hospital with dysarthria and left hemiparesis. On admission he was stuporous with bilateral gaze palsy and left hemiparesis. CT scan on admission showed low density areas in the right cerebellar hemisphere and ventricular part of the pons. Right retrograde brachiography revealed occlusion of the basilar artery, aplasia of the right vertebral artery and an abnormal vessel connecting the right external carotid artery and the right vertebral artery. This anastomotic vessel was thought to be a persistent primitive first cervical intersegmental artery (Proatlantal artery II). Left carotid angiography revealed the left posterior cerebral artery was visualized through the posterior communicating artery, leading from the internal carotid artery. Left retrograde brachial angiography showed that the left vertebral artery terminated just distal from the branching of the left posterior inferior cerebellar artery. After admission the left hemiparesis deteriorated gradually and tracheotomy was done due to respiratory difficulties. The patient was then transferred to the rehabilitation center on his 34th day in hospital with neurological deficits.     

Cerebral arteritis and cerebritis caused by subdural empyema: two cases report]

We report two cases of cerebral angitis and cerebritis caused by subdural empyema. A 22-year-old man, who complained of a headache and high fever, suddenly developed unconsciousness and right hemiparesis. CT and MRI demonstrated left subdural empyema with diffuse brain swelling. CT angiography showed diffuse narrowing of the left internal carotid artery, middle cerebral artery, and anterior cerebral artery. Although we performed craniotomy, continuous irrigation with drainage, systemic injection of antibiotics for subdural empyema, antiplatelet therapy, and hyperbaric oxygen therapy for angitis, his condition remained unchanged. A 67-year-old man who had previously undergone burr hole surgery presented to our hospital for the treatment of scalp infection. He suddenly developed unconsciousness and right hemiparesis. CT and MRI demonstrated left subdural empyema with diffuse brain swelling, but MR angiography did not show any abnormal findings. Hemiparesis improved after the surgery and systemic injection of the antibiotics. Subdural empyema with sinusitis or meningitis around the skull base sometimes causes cerebral angitis. We considered that the angiographical evaluation for the subdural empyema was necessary to detect angitis.     

Cerebral embolism following trivial trauma in children--report of three cases]

Three cases of cerebral embolism secondary to trivial trauma are reported. Case 1: A 12-year-old male suffered a severe headache followed by a generalized convulsion after he turned his head when he was flying a kite. A neurological examination on admission demonstrated right hemiparesis and aphasia. A CT revealed a low density in the left putamen, temporal lobe and frontal lobe. Left carotid angiography (CAG) showed irregular narrowing of the internal carotid with an embolic occlusion and narrowing of the middle cerebral artery with the intraluminal presence of emboli both in the anterior and middle cerebral arteries. He is now doing well but has right hemiparesis. Case 2: This 6-year-old female could not grasp chopsticks and had neck pain 10 minutes after being pulled up by the right arm by her father. Neurological examination demonstrated a right hemiparesis and aphasia. A CT scan and magnetic resonance imaging (MRI) of the head showed an infarcted area in the left caudate head, anterior limb of the internal capsule and putamen. Left CAG revealed an obstruction of the trunk of the middle cerebral artery. She has slight weakness in her right extremities. Case 3: This 11-year-old female noted a weakness in her left lower limb soon after her hair was pulled backward. On admission, a neurological examination failed to demonstrate any abnormality. CT showed an ill defined low density lesion in the right putamen. MRI revealed a high intensity lesion in a T2 weighted image. Right CAG showed an irregularity of the arterial wall in the cavernous portion of the right internal carotid artery.(ABSTRACT TRUNCATED AT 250 WORDS)     

A case of primary subarachnoid hemorrhage due to cerebral amyloid angiopathy]

A 77-year-old man who was suffering from an intracerebral hemorrhage of the left subcortex without hypertension was admitted to our hospital. The only neurological symptom was right arm monoparesis. Brain MRI demonstrated a subarachnoid hemorrhage (SAH) in the left frontal lobe. On the day of admission, conventional cerebral angiography revealed no abnormalities in brain arteries. His symptom was disappeared immediately after admission. He was discharged without neurological deficit on day 25. However, he was rehospitalized in our hospital on the same day because he experienced a right subcortical hemorrhage. The neurological symptoms were consciousness disturbance, aphasia and right hemiparesis. Brain CT disclosed a subcortical hemorrhage in the left temporal lobe. CT stereo-guided drainage was performed. Then, we examined tissue removed from the brain's surface. Histologically, beta-amyloid protein was deposited on the walls of the meningeal and cortical vessels, and it replaced all the layers of those walls. Therefore, a diagnosis of cerebral amyloid angiopathy (CAA) was made. His condition gradually improved, but CT showed an asymptomatic ICH in the right parietal lobe on day 36. On day 47, he had a symptomatic ICH in the left caudate nuclei and right frontal lobe. He died on day 66 because of pneumonia. Intracranial hemorrhages due to CAA have been reported and the majority of the lesions have been lober hemorrhage. To the best of our knowledge, few reports have been published regarding primary SAH caused by CAA. The cause of SAH should be considered as CAA when SAH appears without hypertension or in elderly patients.     

Serial magnetic resonance images in patient with the middle cerebral artery dissection]

A 30-year-old man suffered from transient left hemiparesis and was admitted under the clinical diagnosis of transient ischemic attack. Cerebral angiogram on admission disclosed severe stenosis at the horizontal portion of the right middle cerebral artery. Magnetic resonance images (MRI) on axial view showed a linear enhanced lesion along the stenosis. Images on sagittal view disclosed a crescent-like lesion surrounding a flow void of the middle cerebral artery. After administration of aspirin, he had never suffered from hemiparesis. The enhanced lesion of the middle cerebral artery gradually disappeared on MRI. Although the middle cerebral artery showed temporary improvement of the stenotic lesion, it finally occluded 9 months after the onset. A diagnosis of spontaneous dissection of the right middle cerebral artery was made. The process of the arterial hemodynamics, such as a shrinking of the pseudo-lumen and a flow improvement in the true lumen, was well documented on serial MRI with Gd-DTPA and serial MRA.     

Early ischemic lesion demonstrated by ictal diffusion-weighted MRI during prior TIA in a patient with cerebral infarction]

We reported a patient with transient ischemic attack (TIA), subsequently evolving to a cerebral infarction, in whom ictal diffusion-weighted magnetic resonance imaging (MRI) detected early ischemic lesion in the left hemisphere. The patient was a 30-year-old right-handed male medical doctor, who had an in-hospital episode of TIA with obtundation and right hemiparesis, which lasted for 150 minutes. Ictal diffusion-weighted MRI obtained 110 minutes after symptom onset demonstrated an area of high signal intensity in the left striatum and corona radiata, whereas T 2-weighted and FLAIR images were entirely normal. Ictal magnetic resonance angiography (MRA) showed occlusive lesions in the M 2 branches of the left middle cerebral artery. The second MRA obtained 90 minutes after resolution of the symptoms showed nearly complete recanalization of the left middle cerebral artery, suggesting that the TIA was embolic mechanism. However the patient rapidly developed similar neurological symptoms again 58.5 hours after the TIA episode, evolving finally to a completed stroke. A brain CT obtained 1 hour after the second episode demonstrated diffuse hypodense lesions in the left basal ganglia and corona radiata, and in the left temporal lobe. MRIs 3 and 7 days later displayed completed infarcts, of which distribution was consistent with that of the hypodense lesions on the earlier CT. The left middle cerebral artery remained patent on the follow-up MRAs. The patient fairly recovered and returned to his premorbid position as medical doctor with a mild residual right hand clumsiness. In this patient, ictal and post-ictal MRAs documented an occlusion and a reopening of the middle cerebral artery. The embolic mechanism remains unknown despite detailed cardiac, vascular, and hematological examinations. In addition to recurrent embolism, we would like to point out that the reperfusion injury, secondary delayed neuronal death, and other factors may be involved in the second exacerbation evolving to the completed stroke.     

Hyperperfusion Syndrome after Stent/Coiling of a Ruptured Carotid Bifurcation Aneurysm

The authors report a syndrome of regional, symptomatic cerebral hyperperfusion, and edema mimicking infarction in a 54-year-old woman following coiling of a ruptured right carotid bifurcation aneurysm and stenting of the right middle cerebral artery. The patient presented with a Hunt and Hess grade III subarachnoid hemorrhage 7 days after developing thunderclap headache. She underwent successful coiling under general anesthesia of the 1.6 × 1.5 × 1.6 cm aneurysm, but immediately after the coil was placed occlusion of the proximal M1 segment was developed. This occlusion was stented after ~5-min delay, and flow restored without angiographic evidence of distal emboli. Following the procedure, she was extubated and noted to have left hemiparesis, neglect, and mutism without a CT correlate. Cerebral infarction was suspected, but urgent repeat angiography demonstrated patent cerebral vasculature. On the following day, symptoms persisted, and non-contrast head CT now showed cerebral edema localized to the right middle cerebral artery territory mimicking subacute infarction. CT perfusion imaging and angiography showed a widely patent MCA circulation, and suggested a regional hyperperfusion syndrome. The blood pressure was incrementally lowered, with rapid and sustained neurological improvement. Hyperperfusion events following aneurysm repair and related circumstances are reviewed.     

A case of acute cervical epidural hematoma mimicking medial medullary infarction complicated by arterial dissection]

A 67-year woman with hypertension rapidly noted weakness of the right upper and lower extremities with posterior cervical pain. At admission to our hospital, she showed right hemiparesis without facial palsy, and bilateral pathological reflex. Chest X-ray demonstrated enlargement of the mediastinal shadow. We suspected that she developed aortic arch dissection extending into the vertebral arteries and subsequent medial medullary infarction. However, enhanced thoracic CT, brain MRI-DWI and MRA examinations were negative. Her symptoms rapidly recovered three hours after the onset. A cervical MRI study revealed cervical epidural hematoma locating between the C3 and C6, which suppressed right side of the spinal cord. In conclusion, cervical epidural hematoma as well as medial medullary infarction complicated by the vertebral arterial dissection should be urgently explored when a patient had a sudden onset of cervical pain and hemiparesis without facial palsy.     

Recurrence of bilateral spontaneous cervical internal carotid artery dissection after a 12-year-interval: a case report]

Recurrence of spontaneous cervical internal carotid artery (ICA) dissection is not rare (1%/year) but bilateral recurrence affecting the same cervical ICA is rare, especially after a 12-year-interval. A 41-year-old man exhibited left hemiparesis and angiography revealed tapered stenosis of his right cervical ICA. Within 2 days, his hemiparesis improved. After 21 days, repeated angiography showed complete resolution of the once-stenosed right cervical ICA. He was discharged with slight left hemiparesis. The follow-up angiography performed after 18 months disclosed not only the recanalization of the right cervical ICA but also a new concentric stenosis of his left cervical ICA. Since he presented no new neurological deficit, he was treated with an antiplatelet agent. The angiography performed 14 months later revealed normalization of bilateral cervical ICA. After 12 years, at the age of 53, he presented with worsening of his left motor weakness. Also on this occasion, angiography revealed bilateral cervical ICA dissection and their spontaneous resolution. The anamnesis revealed that he had experienced the same ischemic symptoms, that is, hemiparesis, aphasia and their spontaneous resolution, when he was 24 and 37 years of age. These 4 episodes had some characteristics in common: occurrence in winter (from December to March), being preceded by moderate fever and upper respiratory tract infection. The pathogenesis of spontaneous cervical ICA dissection is unclear. From experience with this patient, we propose that the occurrence of spontaneous cervical ICA dissection might depend on a genetic predisposition and infection might play the role of a trigger.     

Obliteration of bilateral dissecting aneurysms of the vertebral arteries following repeated subarachnoid hemorrhage: a case report

A 51-year-old man presented with loss of consciousness when he underwent urological examination at another hospital. CT scans showed subarachnoid hemorrhage, and cerebral angiography showed bilateral dissecting aneurysms of the vertebral arteries. Following ventricular drainage, the lesion was managed conservatively with blood pressure control but again ruptured on day 8. Cerebral angiography revealed narrowing of both the dissecting aneurysms. On day 11, the right vertebral artery had been spontaneously obliterated and the right dissecting aneurysm was filled in a retrograde fashion via the left vertebral artery. Proximal occlusion of the right vertebral artery was performed to prevent recanalization. Two months later, cerebral angiography revealed that both vertebral arteries were obliterated and the basilar artery and right posterior inferior cerebellar artery were filled via the right posterior communicating artery. The present case demonstrated that the hemodynamic status of bilateral dissecting aneurysms of the vertebral artery changed variably indicating the necessity of careful angiographic observation.     

A case of anterior cerebral artery dissection causing enlargement of infarction]

A 46-year-old woman presented with weakness in the right arm and leg. She had developed difficulty in moving the right arm and leg while exercising and had noticed headache simultaneously. On admission, she had hemiparesis of the right side. Angiography on day 1 disclosed irregularity of the left anterior cerebral artery (ACA). We started argatroban and aspirin to prevent exacerbation of ischemia. Diffusion-weighted MR image on day 2 disclosed acute infarction in the territory of the left ACA. When she became able to move her leg against gravity (MMT 3/5), we discontinued antithrobotic therapy on day 3. MRI on day 10 disclosed enlargement of the infarcted area. Angiography on day 16 disclosed stenosis and dilation corresponding to pearl and string sign involving the left ACA. Spontaneous ACA dissection was established based on clinical features and angiographic findings. Antithrombotic therapy in patients with intracranial artery dissection remains controversial because subarachnoidal hemorrhage can complicate the course due to rupture of dissecting aneurysm, for there is no external elastic lamina in intracranial arteries. However, some cases of ACA dissection have showen progression of ischemic symptoms and enlargement of the infarcted area during the acute or subacute phase.     

Dyke-Davidoff-Masson syndrome manifested by seizure in late childhood: a case report.

The patient was a 19-year-old woman who presented with hemiatrophy and diminished superficial sensation on the left side of her body including her face. She had a past history of tonic-clonic seizures accompanied by left hemiparesis in late childhood. Brain CT demonstrated dilatation of the frontal sinus, calvarial thickening, cerebral hemiatrophy and dilatation of the lateral ventricle on the right side. Brain MRI showed atrophy of the right cerebrum and midbrain and dilatation of the lateral ventricle on T1-weighted images, as well as a high signal intensity area from the parietal to the occipital lobe on T2-weighted images. These findings are suggestive of an episode that may have caused a transient ischemia through the right cerebral hemisphere after the intrauterine period.