A case of peduncular hallucination after aneurysmal subarachnoid hemorrhage]

We reported a case of peduncular hallucination after aneurysmal subarachnoid hemorrhage (SAH). The patient underwent endovascular embolization of an intracranial aneurysm using the Guglielmi detachable coils (GDCs) 9 days after SAH. On the 11th day, she reported visual hallucination: a maggot was on the ceiling, or a soldier who wore green clothes was standing by a locker. The hallucination was vivid, well-formed and associated with insomnia, suggesting peduncular hallucination. A computed tomographic (CT) scan revealed small infarctions of right frontal lobe, which were not responsible for the visual hallucination. Hyperdynamic therapy relieved the visual hallucination 23 days after SAH. It was conceivable that vasospasm was the cause of the infarction and visual hallucination. Only 4 cases with peduncular hallucination after SAH were reported in conjunction with vasospasm. The symptom may be concealed by disturbance of consciousness. Visual hallucination should be considered as a sign of cerebral vasospasm, and an appropriate treatment should be done at right time.     

Intracranial Extension of Spinal Subarachnoid Hematoma Causing Severe Cerebral Vasospasm

Spinal subarachnoid hemorrhages (SAH) can extend into the intracranial subarachnoid space, but, severe cerebral vasospasm is rare complication of the extension of intracranial SAH from a spinal subarachnoid hematoma. A 67-year-old woman started anticoagulant therapy for unstable angina. The next day, she developed severe back pain and paraplegia. MRI showed intradural and extramedullar low signal intensity at the T2-3, consistent with intradural hematoma. High signal intensity was also noted in the spinal cord from C5 to T4. We removed subarachnoid hematoma compressing the spinal cord. The following day, the patient complained of severe headache. Brain CT revealed SAH around both parietal lobes. Three days later, her consciousness decreased and left hemiplegia also developed. Brain MRI demonstrated multiple cerebral infarctions, mainly in the right posterior cerebral artery territory, left parietal lobe and right watershed area. Conventional cerebral angiography confirmed diffuse severe vasospasm of the cerebral arteries. After intensive care for a month, the patient was transferred to the rehabilitation department. After 6 months, neurologic deterioration improved partially. We speculate that surgeons should anticipate possible delayed neurological complications due to cerebral vasospasm if intracranial SAH is detected after spinal subarachnoid hematoma.     

A case of infarction in brainstem and cerebellum as a initial symptom with bilateral hearing loss]

A 56-year old male presented with a sudden onset of bilateral hearing difficulty. He complained of dizziness and gait disturbance at the onset and subsequently developed bilateral hearing loss and tinnitus. Brain MRI revealed multiple infarcts in bilateral middle cerebellar peduncles, bilateral cerebellar hemispheres and the right cerebral peduncle. Three dimentional computed tomography angiography (3D-CTA) showed severe stenosis of bilateral vertebral arteries. Infarcts were located in the border zone between anterior inferior cerebellar artery (AICA) and superior cerebellar artery (SCA), suggesting hemodynamic infarctions. Auditory brain stem responses (ABR) were recorded three times. The initial ABR demonstrated all waves except for wave I on day 14. Wave I on the left was normal, while wave I peak latency on the right was prolonged. On day 61, all waves were recorded, although peak latencies of waves III to V and interpeak intervals of the wave I to III on the right side were prolonged. Involvements of the cochlear nerve and pontine auditory pathway were suggested from the ABR abnormalities in this case.     

A case report of bilateral cerebral peduncular infarction manifesting tetraparesis and pseudobalbur palsy]

A 63-year-old female had presented with right hemiparesis and slight dysarthria. MRI had showed the infarction of left pons and left peduncle. Three months later she further presented with left hemiparesis, severe dysarthria and swallowing disturbance. MRI showed bilateral cerebral peduncular infarction. And the angiogram showed the occlusion of basilar artery at the just distal portion of the superior cerebellar artery. We recognized our case as the infarction due to the basilar artery occlusion. The 16 cases of bilateral cerebral peduncular infarction were reported. In these reports, the symptoms of bilateral cerebral peduncular infarction were locked-in syndrome in 15 cases and persistent vegetative state in only one case. Our patient presented with tetraparesis and pseudobalbur palsy not with locked-in syndrome, probably because the area of infarction was limited within almost lateral portion of peduncle. The sparing of posterior cerebral artery was one of the reason of such a condition. This is the first report of bilateral cerebral peduncular infarction manifesting tetraparesis and pseudobalbur palsy.     

A case of brain stem infarction with bilateral hearing loss]

The study case was a 66-year-old man who had bilateral neurosensory hearing impairment due to brain stem infarctions. He noticed mild hearing loss, frequent vertigo and tinnitus. About one month later, his hearing took a sudden turn for the worse, and he suffered from dysarthria, dysphagea and abasia. Neurological examination revealed pseudobulber palsy, left hemiparesis, cerebeller ataxia, disturbance of pain and temperature sensation on the right face and left side of the body. Brain stem auditory evoked potentials (BAEPs) showed a delayed small wave V with the abscence of previous waves on the right side and no significant waves on the left side. Brain magnetic resonance images (MRI) revealed infarctions in the bilateral middle cerebellar peduncles, including in the right lateral portions of pons, and the right lower pontine base. We believe that not only peripheral, but also central auditory pathways adjacent to infarctions were damaged. Magnetic resonance angiography (MRA) showed severe stenosis or occlusion of left vertebral artery and basilar artery. We concluded that hypoperfusion of the vertebrobasilar artery territories caused ischemia of the cochlear nerve and the auditory tracts in the brain stem, which resulted in bilateral hearing loss.     

Multiple cerebral embolism caused by a patent foramen ovale and a uterine myoma]

Recently, patent foramen ovale(PFO) has been highlighted as an important risk factor of cerebral infarctions in young adults. We report a patient of multiple cerebral embolism associated with PFO and deep venous thrombosis caused by a uterine myoma. A 40-year-old woman suddenly suffered from right hemiparesis with motor aphasia. Brain angiography showed an occlusion of M2 portion of the left middle cerebral artery, but atherosclerotic changes were not seen. She developed left facial paresis 23 days later and admitted to our hospital. Brain MRI revealed multiple cerebral infarcts in the left insular cortex, the deep white matter of the right frontal lobe, and bilateral thalamus. Hypoxia with the perfusion defects of S1 and S2 sections of the right lung demonstrated by scintigraphy suggested pulmonary embolism. Transesophageal echocardiography showed a PFO with spontaneous left-to-right shunt and right-to-left shunt evoked by the Valsalva maneuver. Although venography could not detect thrombi, it revealed severe compression of the right external iliac vein by a uterine myoma. These findings suggested thrombi in the right external iliac vein were the embolic source when combined with elevated coagulation markers. An uterine myoma should be considered as an important risk factor for an embolic source in case of cerebral embolism with PFO.     

A case of transient parkinsonism due to mesencephalic hemorrhage]

A 68-year-old man was admitted because of sudden onset gait disturbance and bradykinesia. He experienced left putaminal bleeding following mild right hemiparesis and emotional incontinence without any difficulties in his daily life since three years before admission. On neurological examination the patient was alert and oriented. He showed forced crying. Myerson's sign was positive. There were no abnormal findings in ocular movements, pupillary reflexes and other cranial nerves. Muscle tone was increased with cog-wheel phenomenon in bilateral upper extremities. Coordination was preserved. He showed severe akinesia and small steppage gait with stooped posture. Freezing phenomenon was observed in initiation of gait and turning. The deep tendon reflexes were increased in the right side with bilateral pathological reflexes. There was no definite weakness and sensory disturbance in all extremities. Brain CT revealed a small high density lesion in the medial side of right cerebral peduncle and a lens-shaped low density lesion in the left putamen. On T1 and T2 weighted images of MRI, right peduncular lesion showed low signal. It extended to the substantia nigra which was partially destructed. His parkinsonism was rapidly improved and completely disappeared within following two weeks. High density lesion of right peduncle on CT also disappeared. We discussed the mechanisms of parkinsonism following unilateral mesencephalic hemorrhage in this patient.     

Benedikt and "plus-minus lid" syndromes arising from posterior cerebral artery branch occlusion

A 53-year-old man was admitted with diplopia, right ptosis, left lid retraction, mild left sided weakness and involuntary movements. Neurological examination revealed plus-minus lid and Benedikt's syndromes together. Magnetic resonance imaging (MRI) showed two distinct mesencephalic infarctions in territories of paramedian and pedincular perforating arteries. Magnetic resonance angiography (MRA) showed severe stenosis of proximal segment of the right posterior cerebral artery (PCA). Rare clinical presentations such as Benedikt and plus-minus syndromes can be seen together and be due to stenosis of the posterior cerebral artery with specific regional infarctions.     

Fibromuscular dysplasia of the basilar artery presenting as cerebral infarction in a young female]

We reported a 20-year-old woman with fibromuscular dysplasia (FMD) of the basilar artery presenting multiple cerebral infarctions. A sudden onset of consciousness disturbance and right hemiparesis was experienced. A neurological examination on day 2 revealed an absence of light and corneal reflexes on the left side, homonymous left upper quadrant anopsia and right hemiparesis with Babinski sign: she was also somnolent. On head MRI, multiple high signal intensity lesions were seen in the right occipital lobe, bilateral thalami and left pons on T2- and diffusion weighted images. Brain angiogram revealed the string of beads sign of the basilar artery, suggesting FMD. Neurological deficits gradually improved in the 2 months that followed, leaving slight hemiparesis and homonymous left upper quadrant anopsia In the following 3 years, no recurrence was seen with aspirin (81 mg/day). FMD in the head and neck usually affects extracranial segments of the carotid and vertebral arteries, while FMD of the basilar artery is extremely rare. To the best of our knowledge, 12 cases with FMD of the basilar artery have been reported; of these, 11 were symptomatic and 5 died. Since FMD of the basilar artery has poor prognosis, attention needs to be paid for FMD in young adults as a differential diagnosis of cerebral infarction in the territory of the basilar artery.     

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.     

Ischemic Stroke with Protein S Deficiency Treated by Apixaban

A 57-year-old man with atherosclerosis obliterans was admitted with sudden-onset sensory aphasia and right hemiparesis. Brain MRI revealed acute cerebral infarctions in the left temporal lobe and magnetic resonance angiography showed occlusion of the posterior branch of the left middle cerebral artery. Transesophageal echocardiography and ultrasonography respectively confirmed a patent foramen ovale and deep vein thrombosis in the bilateral femoral veins. Blood findings showed low protein S antigen, low protein S activity, and a missense mutation of the PROS 1 gene. The administration of apixaban 10 mg BID prevented ischemic stroke recurrence and decreased the deep vein thrombosis. These outcomes indicated that apixaban may be alternative to warfarin for the secondary prevention of ischemic stroke in a patient with a protein S deficiency.     

Persistent primitive trigeminal artery presenting with Weber's syndrome: report of a case with three-dimensional CT angiographic evaluations]

We report a rare case of persistent primitive trigeminal artery(PPTA) presenting with brain stem infarction known as Weber's syndrome, and document its unique findings of three-dimensional CT angiography(3 D-CTA). A 69-year-old woman was admitted to our hospital because of gait disturbance and blepharoptosis on the right eye. Neurological examination on admission revealed the right oculomotor nerve palsy, left hemiparesis and dysarthria, all of which indicated the signs and symptoms of Weber's syndrome. Initial CT scan revealed no abnormality, but a subsequent 3 D-CTA demonstrated the PPTA originating from the right internal carotid artery penetrate into the clivus directly to the distal basilar artery, on top of which a small saccular aneurysm was incidentally visualized. Right internal carotid angiograms showed the PPTA run between the cavernous segment of the internal carotid artery and the distal portion of the basilar artery with the filling of both the posterior cerebral and superior cerebellar arteries. However, the proximal portion of the basilar artery was visualized through the right vertebral artery and there was no blood flow to its distal portion. Evidence of infarction was finally confirmed at the right midbrain and thalamus by the MRI performed 5 days after the onset. With a conservative treatment including physical therapy, the patient recovered well from the deficits and could walk by herself with a cane. With regard to the pathogenesis of vertebrobasilar insufficiency in a patient with PPTA, it is generally considered that microembolus from an atherosclerotic carotid artery may be its cause because of the presence of direct communication between the anterior and posterior circulations. In the present case, however, this mechanism may not be applied since there was no evidence of atherosclerotic plaque or stenotic lesions on the carotid arteries. Alternatively, an embolic occlusion may have occurred in the paramedian branches of the posterior cerebral artery since a dilated PPTA itself, which resembled fusiform-aneurysm in appearance, may become the origin of microembolus.     

A case of lobar cerebral hemorrhage with low concentration of CSF cystatin C

A 49-year-old male was admitted to our hospital because of severe headache and dizziness which had occurred suddenly one day before admission. There was no past history contributory to cerebral hemorrhage but was family history of cerebrovascular accidents in his father and brother. Neurological examination revealed left homonymous hemianopsia, mild left hemiparesis, and left side hemi-neglect in simultaneous stimuli on bilateral extremities. Laboratory data including peripheral blood cells, coagulation tests, and serum chemistry were unremarkable. Brain CT and MRI demonstrated large lobar hematoma in the right parieto-occipito-temporal region. Cystatin C level in the CSF samples taken on the 39th and 59 th days (38 and 27 ng/ml respectively) were low, compared with the normal value (greater than 100 ng/ml). These findings suggest that the lobar cerebral hemorrhage of the present case might have been caused by cerebral amyloid angiopathy with cystatin C deposits.     

A case of convexity subarachnoid haemorrhage from intracranial hypotension treated with epidural blood patch

The majority of subarachnoid haemorrhages (SAH) are of aneurysmal origin, and nontraumatic convexity SAH is rare. We describe one patient who had a convexity SAH caused by cortical veins thrombosis (CVT) secondary to intracranial hypotension (IH). We discuss possible pathophysiologic mechanisms and its treatment. A 52-year-old female presented with left hemiparesis and tonic–clonic seizures, following lumbar epidural injections of local anaesthetics and steroids because of chronic low back. Brain CT showed right fronto-parietal convexity SAH. Brain MRI revealed diffuse pachymeningeal enhancement and confirmed the SAH. Cerebral angiography showed no/low flow signal in few frontal and parietal cortical veins in the correspondence of the SAH. A restoration of flow signal in this area was revealed after 2?months. The patient was treated with lumbar epidural blood patch with recovery. Convexity SAH caused by CVT from IH may be treated only with lumbar epidural blood patch which eliminates by itself the determinants of CVT (vein dilatation and slow vein drainage).     

A case of bilateral cerebellar infarction in the distribution of the bilateral superior cerebellar artery]

We reported a case of bilateral cerebellar hemorrhagic infarction in the distribution of the bilateral superior cerebellar artery. A 58-year-old man suddenly developed dizziness and transient loss of consciousness. The neurological examination revealed left hearing disturbance, left sensory disturbance involving face, dysarthria and bilateral ataxia. This patient was considered to be classic clinical syndrome of right superior cerebellar artery. CT and MRI revealed hemorrhagic infarction corresponding to the full territory of the bilateral superior cerebellar artery. The right posterior cerebral artery was filling through the right posterior communicating artery on the right carotid angiography taken 2 hours after the onset. Bilateral vertebral angiography on the 18th day demonstrated no occlusions in the basilar artery and the bilateral superior cerebellar artery. Hemorrhagic infarction corresponding to the full territory of the bilateral superior cerebellar artery, sparing other territories as the present case, is extremely rare. In this case, cerebral embolism (top of the basilar syndrome) was suggested because of existence of atrial fibrillation and sudden onset.     

Bilateral chronic subdural hematoma in a young adult mimicking subarachnoid hemorrhage]

A 33-year-old man was admitted to our hospital with a sudden severe headache five days after the onset CT scan showed a slight high-density area in the basal cistern, mimicking subarachnoid hemorrhage (SAH), and diffuse brain swelling. However, conventional cerebral angiography and CT angiography failed to demonstrate aneurysms and vascular malformations. MRI showed bilateral subdural hematoma, but no SAH. Irrigation of liquefied subdural hematoma, causing high intracranial pressure, was carried out. Postoperative course was uneventful and his headache resolved within a day. The author presented a case of bilateral chronic subdural hematoma who presented with a sudden severe headache mimicking a SAH. Hyper attenuation in the basal cistern and subarachnoid space in CT, don't always indicate SAH. MRI, including fluid-attenuated inversion recovery (FLAIR) sequences, is useful in differentiating the "pseudo" SAH from "true" SAH, and lead to the right diagnosis.     

Post-partum cerebral angiopathy: repetitive TCD,MRI, MRA,and EEG examinations

We report of a woman with post-partum cerebral angiopathy (PCA), in whom we repetitively performed transcranial Doppler sonography (TCD), MR imaging (MRI), and MR angiography (MRA) to evaluate the underlying pathophysiology. A 31-year-old woman, Gemini pregnant, complained of severe throbbing frontal headache four days after an uneventful delivery by Cesarean section. Blurred vision occurred eight days after delivery, followed by three generalized tonic-clonic seizures. Neurological examination revealed a somnolent woman without focal neurological deficits. At the day of the seizures increased flow velocities and disturbed flow were observed in the right posterior and anterior cerebral artery on transcranial Doppler (TCD). MRI showed infra- and supratentorial patchy hyperintensities in T2-weighted images and in the FLAIR sequence. Diffusion-weighted imaging revealed corresponding multi-focal hyperintense areas indicating increased diffusion and MRA showed a diffuse multisegmental narrowing of all pial arteries. MRI at day 10 was completely normal, but MRA still revealed vascular narrowing in the right posterior cerebral artery. General slight flow accelerations in all basal arteries occurred after 10 days and lasted for three weeks. PCA is apparently associated with a vascular narrowing causing cerebral ischemia with increased diffusion. Later reactive cerebral hyperperfusion is observed. Vascular narrowing and cerebral hyperperfusion still persist after MRI has normalized.     

Bilateral multiple border zone infarctions after massive bleeding: report of two cases]

We present two patients who developed bilateral border zone brain infarctions after massive bleeding. Patient 1 was a 46-year old woman who developed bilateral visual disturbance and left hand monoparesis after excessive menstruation with severe anemia. Diffusion-weighted MRI of brain showed multiple border zone infarcts bilaterally in cerebral and cerebellar hemispheres while brain MRA was normal. Patient 2 was a 67-year old man who developed disturbance of consciousness and right hemiplegia after upper gastrointestinal tract bleeding. Diffusion-weighted MRI of brain showed bilateral multiple border zone infarcts in cerebral hemispheres, although he had asymptomatic occlusion of the left internal carotid artery. The bilateral multiple border zone infarcts are one of the key findings suggesting the presence of anemic hypoxia as a result of global brain hypoperfusion caused by massive blood loss.     

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.     

The influence of ruptured cerebral aneurysm localization on the blood flow velocity evaluated by transcranial Doppler ultrasonography

The relationship between changes of blood flow velocities in cerebral arteries measured by transcranial Doppler ultrasonography and aneurysm localization was investigated in a group of 165 patients after aneurysmal subarachnoid hemorrhage (SAH). Mean blood flow velocities (MFV) in the middle cerebral artery (MCA) and anterior cerebral artery (ACA) were registered. In patients with aneurysm of internal carotid artery and MCA (group A) statistically significant higher values of MFV from the 1st to the 5th day and on the 12th, 13th, 14th, 15th, and 19th day after SAH were found compared to patients with aneurysm of the anterior communicating artery, ACA, and pericallosal artery (group B). Pathological values of MFV exceeding 120 cm sec-1 in MCA were registered during 14 days in group A and during eight days in group B. Blood flow velocities in ACA were statistically significantly higher in group B on the 2nd, 7th, 9th and 11th day compared to group A. Pathological values of MFV exceeding 90 cm sec-1 in ACA were registered during nine days in both groups. MFV differences between group A and group B in 38 patients subjected to delayed surgery were not observed. The influence of aneurysm localization was observed between the 7th and 14th day after SAH. Critical MFV values for vasospasm in the MCA should be 120 cm sec-1 and in the ACA 90 cm sec-1.