Interhemispheric subdural empyema in a patient with allergic rhinitis, pansinusitis and acute excerbation of frontal sinusitis

We reported a 10-year-old boy with an interhemispheric subdural empyema caused by acute excerbation of frontal sinusitis. He has suffered from allergic rhinitis and pansinusitis for years. He had fever and a generalized tonic-conic seizure, followed by prolonged consciousness disturbance and right hemiparesis. CT and MRI were useful to diagnose an interhemispheric subdural empyema, which showed a characteristic double-layer fluid collection pattern. Prompt diagnosis and treatment with craniotomy resulted in recovery without any neurological sequelae. His basic disorders, allergic rhinitis and pansinusitis, were successfully treated with macrolides and antiallergic drugs: pranlukast hydrate and sodium cromoglicate, administered per os and by inhalation, respectively.     

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.     

Acute subdural empyema due to peptostreptococcus]

A very rare case of acute subdural empyema due to peptostreptococcus was reported. A 11-year-old-girl was admitted to our hospital with high grade fever, unconsciousness and rt hemiparesis. CT scans showed the mass effect caused by the subdural empyema over the left frontotemporal region. Subdural empyema was evacuated by the craniotomy. Peptostreptococcus was found in the pus obtained during the operation. However, CT scans 10 days after the operation revealed another subdural empyema in the left frontal base and interhemispheric fissure, which was removed again by the craniotomy using coronal incision 14 days after the first operation. Frontal sinusitis was also demonstrated by CT scan. Killian's operation to the frontal sinusitis was performed by otorhinolaryngologists at the same time. Six weeks after the second operation, she was discharged without any neurological deficits. Peptostreptococcus is one of the indigenous microflora of the oral cavity, skin, gastrointestinal tract and genitourinary system and may be a causative microorganism in every type of human infection due to its abnormal localization. There is a controversy concerning surgical management subdural empyema. Both the burr hole drainage of pus and the craniotomy are advocated. Associated otorhinologic lesions must not be overlooked. Otorhinologic consultation should immediately be obtained so that the drainage of an infected paranasal or mastoid sinus can be performed at the time of craniotomy. This is critical to prevent the recurrence of the subdural empyema from further extension of the extracranial disease.     

老年性大脑纵裂硬膜下血肿

目的 加强对大脑纵裂硬膜下血肿的认识。方法 对3例大脑纵裂硬膜下血肿患者临床资料进行回顾性分析。结果 3例均为男性，年龄分别为78岁、70岁、74岁；1例为自发性，2例为外伤性；发病后临床表现为头晕、头痛、恶心、呕吐、行走不稳、大脑镰综合征(对侧单瘫或以下肢为重的偏瘫)、或短暂意识障碍等，并有延迟出现的特点；2例经复查头部CT确诊，1例经复查头部CT及MRI确诊，均经保守治疗后康复出院。结论 本病头部CT、MRI具有特征性表现，且头部MRI更具敏感性，结合大脑镰综合征可以确诊，治疗及预后取决于病情严重程度。     

Garcin syndrome in a patient with rhinocerebral mucormycosis]

Garcin syndrome is characterized by an unilateral cranial nerves involvement without sensory or motor long-tract disturbances. It is usually caused by tumor infiltrating in the skull base with osteolytic changes on radiological study. We report a case of 64-year-old man with history of alcohol overintake, who admitted local hospital, because of right periorbital edema and facial swelling. He noted right ptosis 2 weeks prior to admission. Neurological examination revealed right multiple cranial nerves involvement including II, III, IV, V, and VI cranial nerves. MR imaging of the brain showed marked paranasal sinusitis and abnormal infiltration of right orbital fat. Orbital apex syndrome related to paranasal sinusitis was diagnosed, and antibiotics was administered. But a few days after admission, he developed a right VII, IX, X cranial nerve palsy. He was transferred to our hospital because of acute development of left hemiparesis and deteriorated consciousness. MR imaging of the brain showed right internal carotid artery (ICA) occlusion, and infarction in right middle cerebral artery (MCA)'s territory. The diagnostic biopsy of the paranasal sinus showed mucorales hyphae, indicating that the pathological diagnosis was mucormycosis. Despite of antibiotic therapy included of amphotericin-B administration and strict control of diabetic mellitus, his sinusitis was gradually spread. His condition progressively deteriorated, and finally died of sepsis. Post-mortem examination revealed a widespread mucor infiltration in the dura mater without skull bone invasion. This case presented with unilateral multiple cranial nerve involvements (Garcin syndrome) followed by left hemiparesis associated with rhinocerebral mucormycosis. It is suggested that mucormycosis should be considered in case of Garcin syndrome without osteolysis in the skull base.     

A case of pontine hemorrhage showing hemiasomatognosia]

We reported a case of pontine hemorrhage showing hemiasomatognosia. A 74-year-old, right-handed man was admitted to our hospital complaining of numbness of left upper and lower extremities. Neurological examination revealed marked disturbance of superficial and deep sensation of left half of his body without hemiparesis and consciousness disturbance. Neuropsychologically, he had experience of having lost the perception of his left upper limb, which was referred to "conscious hemiasomatognosia" by Frederiks. Brain CT and MRI showed a pontine hematoma involving the right medial lemniscus, the right spinothalamic tract and the right medial longitudinal fasciculus. One week after the onset, hemiasomatognosia disappeared with improvement of sensory disturbance. These indicate that this form of hemiasomatognosia may be associated with transient blockage of somesthetic input.     

Spinal subdural empyema diagnosed by MRI and recovered by conservative treatment

Localized suppuration involving the spinal cord is uncommon. A case of spinal subdural empyema is reported. The patient is 54-year-old male who had been suffering a diabetes mellitus but did not receive any treatment. His initial symptom was lumbago. Then he noticed a palpitation and general malaise which made him visit a hospital. Because he did not show any improvement by a fluid therapy, he was transferred to our institute for the further evaluation. On admission, physical examination showed no abnormality. Blood pressure was 170/90 mmHg, heart rate 128/min. and body temperature 37.1 degrees C suggesting a septic shock state. Neurological examination revealed slight consciousness disturbance, mild tetraparesis and bilateral hypesthesia lower than the level of L3. Laboratory examination showed the elevated leukocyte count and fasting blood sugar and urine ketone body levels of 20,500/mm3, 257 mg/dl and 226 mg/dl respectively. Blood culture proved a septicemia of Streptococcus agalactiae afterwards. On the second day of admission, lumbar puncture revealed a purulent cerebrospinal fluid, though X-ray CT of lumbar spine did not confirm a diagnosis. Spinal magnetic resonance imaging (MRI) revealed a widespread abnormal intensity of the spinal canal from the level of Th11 to L4. On the T1-weighted image (TR 300 msec., TE 40 msec.), cerebrospinal fluid space was abnormally isointense. On the T2-weighted image (TR 2,000 msec., TE 80 msec.), subdural and cerebrospinal space was filled with an abnormal high-intense lesion especially on the ventral side. He developed semicoma due to hydrocephalus following a intraventricular empyema. He was also complicated disseminated intravascular coagulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Case of rheumatoid meningitis: findings on diffusion-weighted image versus FLAIR image]

We report a 63-year-old man with rheumatoid meningitis. At 47-years-old, he developed rheumatoid vasculitis causing arthralgia and skin ulcer. Although the patient had been treated with prednisolone and cyclosporine A, headache and recurrent focal seizures of the right upper limb and generalized seizures developed. Brain magnetic resonance imaging showed high signal intensity lesions on FLAIR MRI and associated abnormal enhancement of the leptomeninges. Part of the lesions also showed patchy high signal intensity on diffusion-weighted imaging (DWI). This features may be useful for differentiating rheumatoid meningitis from subdural empyema, because the extent of the lesions on DWI matches the lesion on FLAIR imaging in patients with subdural empyema. Cerebrospinal fluid analysis revealed monocytic pleocytosis and negative findings for infection or malignancy. After intravenous administration of methylprednisolone (1,000 mg/day for 3 days), the patient showed improvements in headache, cerebrospinal fluid findings and abnormal hyperintensity on DWI. Rheumatoid meningitis is an extremely rare neurological manifestation, but careful attention should be paid even in the inactive stage of rheumatoid arthritis. This disease tends to present with unilateral supratentorial lesions. In this case, serial diffusion-weighted and FLAIR MRI was useful for following the leptomeningeal lesions.     

A case of intracranial hemorrhage in a young infant due to vitamin K deficiency: comparison of MRI and CT findings

We reported a case of intracranial hemorrhage due to vitamin K deficiency in a 43-day-old male infant whose MRI findings were compared with CT findings. The infant was vacuum delivered at the 40th gestational week and Apgar score was 9 at 5 min after birth. He weighed 2,750 g at birth and was breast-fed. His growth was normal after birth, but forty-one days after birth, the infant became febrile and vomited three times. Forty-two days after birth, right hemiconvulsions occurred and the infant vomited again. He was brought to our clinic forty-three days after birth, because cranial CT showed multiple intracranial hemorrhages. On admission, skin color was pale, and the patient was somnolent. The anterior fontanel was bulging and tense. Neurological examination revealed right hemiparesis. Since laboratory data indicated that intracranial hemorrhage resulted from vitamin K deficiency, administration of vitamin K and blood transfusion were carried out. MRI examination was made three days after admission, and demonstrated a posterior fossa subdural hematoma as well as a left frontal subdural hematoma associated with intracerebral hemorrhage. Five days after admission, left frontal subdural hematoma was removed by left frontal craniotomy, and twenty-six days after the operation he was discharged without any neurological deficits.(ABSTRACT TRUNCATED AT 250 WORDS)     

A case of subdural empyema with transient cerebral white matter lesions

We reported a fourteen years old male with subdural empyema followed by consecutive magnetic resonance imaging (MRI) examination. He was admitted to our hospital, complaining incomplete paresis of the left upper extremities, headache and high fever. The first MRI T2-weighted image at admission revealed an abnormal high intensity in the right frontal subdural space, indicating an abscess. Antibiotics therapy and a burr hole operation were effective and he made a remarkable recovery. One month later, the third MRI T2-weighted image showed an abnormal high intensity in the deep white matter of the right frontal lobe, which had not been detected in the subsequent MRI after the operation. On the other hand, the meningeal enhancement on the second Gd-DTPA enhanced MRI was more thickened than the previous meningeal enhancement. This abnormal high intensity on MRI had disappeared two month later, when the meningeal enhancement had grown thin. These data suggested the meningeal enhancement was relative to the transient high intensity which was considered to represent brain edema. We concluded that careful observation and serial MRI examination might be necessary in patient with subdural empyema even after disappearance of all symptoms.     

Magnetic resonance imaging findings of Kernohan-Woltman notch in acute subdural hematoma.

OBJECTIVE AND IMPORTANCE: We report the case of a 73-year-old patient who presented a right motor deficit caused by an ipsilateral acute subdural hematoma. A magnetic resonance imaging (MRI) demonstration of Kernohan-Woltman notch phenomenon was obtained. CLINICAL PRESENTATION: The woman sustained a major head injury at home, followed by loss of consciousness. On admission to the emergency room, she was comatose, anisochoric (left > right), and showed a reaction to pain with decerebrating movements of left limbs (Glasgow Coma Scale (GCS) 4/15). A right severe hemiparesis was observed. Cerebral computed tomography scan showed a large right hemispheric subdural hematoma. INTERVENTION AND POST-OPERATIVE COURSE: A wide right craniotomy was performed and the subdural hematoma evacuated. During the post-operative period, the level of consciousness gradually improved. A MRI performed about 2 weeks after operation showed a small area of abnormal signal intensity in the left cerebral peduncle. On discharge, the woman was able to communicate with others, but her right hemiparesis was still severe.     

Cortical deafness following bilateral hypertensive putaminal hemorrhage

A case of cortical deafness is reported, which was caused by two episodes of bilateral hypertensive putaminal hemorrhage. Such a case has not appeared in literature up to this time. The patient was a right-handed, 69-year-old man, admitted to us after the stroke with right hemiparesis and disturbance of consciousness. CT scans showed right putaminal hemorrhage. After recovery of consciousness, the patient complained of hearing difficulty of the right ear. The right hemiparesis improved and he was followed ambulatorily after two months hospitalization. He returned to his work and was able to drive a car. His hearing difficulty of the right ear progressed and became stone deaf six months after onset of the initial stroke. Two years after the first stroke, he was attacked by the second stroke with left hemiparesis. CT scans showed left putaminal hemorrhage larger than the previous one in the right. When the patient recovered consciousness, he complained of total deafness. Audiometry test showed that hearing was lost completely to both high and low notes, and there was absence of bone conduction bilaterally. Auditory brain stem response test revealed normal pattern from wave I through wave V bilaterally. Middle latency response showed normal component Po on the right ear and it was absent on the left. The component Pa was not identified on both ears. He showed skill and reliance on lip reading two years after the onset of the complete deafness. Now he can speak fluently and communicate with lip reading and written language, although no improvement of the complete deafness being noticed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Kernohan-Woltman notch phenomenon caused by an acute subdural hematoma

Uncal herniation through the tentorial notch is occasionally associated with false localizing ipsilateral hemiparesis, known as the Kernohan-Woltman notch phenomenon (KWNP). We report an 81-year-old female who presented with a decreased level of consciousness, a right mydriasis and an ipsilateral motor deficit caused by a large right hemispheric subdural hematoma that was immediately evacuated. The patient recovered well, although her right hemiplegia persisted. A follow-up MRI showed a residual lesion in the left cerebral peduncle, corresponding to KWNP. The presence of such a structural lesion suggests a poor prognosis for recovery from the initial motor deficit.     

Rapidly progressive lumbar subdural empyema following acromial bursal injection

Spinal subdural empyemas are rare. We describe a 53-year-old male who presented with back pain, mental status changes, and sepsis. Five days prior he had undergone a triamcinolone and lidocaine injection of the acromial bursa. He also had a remote history of epidural steroid injection for thoracic back pain. Two lumbar MRI conducted 62 hours apart revealed a newly developed subdural empyema that was successfully treated with surgical evacuation and post-operative antibiotics.     

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.     

Kernohan's notch phenomenon in chronic subdural hematoma: MRI findings.

We report two cases of Kernohan's notch phenomenon secondary to chronic subdural hematoma detected by MRI. In the first case, the patient was drowsy with an oculomotor palsy and a hemiparesis ipsilateral to the chronic subdural hematoma. MRI in the post-operative period showed no abnormal signal or deformity of the crus cerebri. The neurological signs immediately resolved after trephination. In the second case, the patient was admitted with progressive decrease in their level of consciousness and ipsilateral hemiparesis with the chronic subdural hematoma. MRI on admission revealed an abnormal signal in the contralateral crus cerebri against the chronic subdural hematoma. After surgery, the mental state gradually recovered to normal with some degree of residual hemiparesis. In patients with chronic subdural hematoma, a compressive deformity of the crus cerebri, without abnormal signal on MRI, may predict a better neurological recovery in patients with Kernohan's notch phenomenon.     

Diffusion-weighted magnetic resonance imagings at the acute stage in two patients with spectacular shrinking deficit due to cardioembolic stroke]

We report diffusion-weighted magnetic resonance imagings (DWI) at the acute stage of two patients with spectacular shrinking deficit (SSD) due to cardioembolic stroke. Patient 1 was a 74-year-old woman with atrial fibrillation (Af) who had been admitted for acute cholecystitis. She abruptly developed consciousness disturbance, global aphasia and right hemiparesis. Her neurological symptoms rapidly improved 30 minutes after onset, and completely disappeared in four hours. Patient 2 was a 84-year-old woman with Af who had been on medication of warfarin potassium for three years. She abruptly developed consciousness disturbance and left hemiplegia. Her neurological symptoms rapidly improved 90 minutes after onset, and almost completely disappeared in ten hours. Their conditions were consistent with SSD in acute cardioembolic stroke. DWI of Patient 1 taken 27 hours after onset showed hyperintense signal areas in the insular and temporal cortices of the left middle cerebral artery territory, and in the parietal cortex corresponding to the border zone between the territories of the left middle cerebral artery and posterior cerebral artery. DWI of Patient 2 taken 39 hours after onset showed hyperintense signal areas in the insular and frontal cortices of the right middle cerebral artery territory, and in the parietal cortex corresponding to the border zone between the territories of the right middle cerebral artery and posterior cerebral artery. They indicated multifocal ischemic injuries at the acute stage. The T2-weighted MRI of Patient 2 showed a slight hyperintense signal area only in the right parietal cortex, but the fluid-attenuated inversion recovery (FLAIR) in both patients showed no abnormal signals in the corresponding areas. To our knowledge, ischemic lesions in DWI of SSD at the acute stage after rapid recovery have not been reported previously. DWI is useful in SSD for detecting ischemic injuries of cardioembolic origin at the early stage.     

Thrombosed vertebral artery aneurysm presenting with hemorrhage and bulbar compression: report of two cases

Bulbar compression by vertebral artery (VA) aneurysm is extremely rare and only reported in a few cases. We report two cases with thrombosed VA aneurysm compressing medulla oblongata; one presented with bulbar apoplexy hemorrhage and the other with subarachnoid hemorrhage (SAH). A 61-year-old male (case 1) presented with consciousness disturbances, left hemiplegia, and subsequent respiratory arrest. He was subjected to controlled ventilation, and computed tomography (CT) scan showed bulbar hemorrhage. Magnetic resonance imaging (MRI) and digital subtraction angiogram (DSA) revealed fusiform right VA aneurysm with partial thrombosis and bulbar compression. Intra-aneurysmal embolization with Guglielmi detachable coils (GDCs) relieved his clinical symptom including respiratory disturbance. Three months after the onset, he remained moderately disabled. A 76-year-old male (case 2) presented with severe headache and subsequent respiratory disturbance. CT scan on admission showed subarachnoid hemorrhage with acute hydrocephalus. Ventricular drainage rapidly improved consciousness while respiratory disturbance persisted over several days. MRI and DSA suggested spontaneous thrombosis of the right VA dissection with bulbar compression. He showed gradual recovery of his respiration over a week. After ventriculo-peritoneal shunting, he was transferred with moderate disability. These results suggest that the elimination of the pulsatile effect of VA aneurysm adjacent to medulla oblongata can improve symptoms caused by aneurysm-related compression. Early diagnosis and appropriate treatment such as intra-aneurysmal embolization for ameliorating the blood flow inside the aneurysm can relieve mass effect and clinical symptoms.     

Thyrotoxic encephalopathy showing reversible diffusion-weighted imaging abnormalities]

A 31-year-old man was transferred to our emergency room (ER) with acute onset of high-grade fever and consciousness disturbance. His consciousness at ER was severely disturbed with restlessness. No apparent focal neurological signs were seen. MRI with diffusion-weighted images (DWI) showed high signal intensities at the corpus callosum, left cerebellar hemisphere, left deep white matter and right middle cerebellar peduncle. These lesions were low signals in apparent diffusion coefficient(ADC) map, indicating cytotoxic edema. EEG showed enhanced fast waves seen in predominantly frontal regions. CSF examination was normal except elevated initial pressure of 210 mmH2O. He was treated with high dose dexamethasone and acyclovir. His consciousness and high-grade fever with systemic inflammatory responses were dramatically improved after these treatments. Subsequent data showed hyperthyroidism with anti-thyroid stimulating hormone receptor antibodies. This case was thought to be a thyrotoxic encephalopathy with beneficial response to corticosteroid therapy. Abnormalities seen in DWI and EEG were normalized ten days later.     

Extensive subdural empyema treated with drainage and barbiturate therapy under intracranial pressure monitoring: case report

In subdural empyema (SDE), if the mass effect and vasogenic edema are not controlled, the brain can be fatally damaged. Massive SDE over the skull base often requires repeated surgical drainage for removal of accumulated pus. Intracranial pressure (ICP) management until obliteration of the empyema is important to the improvement of clinical outcome. An 18-year-old man was admitted to our center in a nearly comatose state and with a mild fever. CT scan showed massive SDE extending to the skull base and parafalx. ICP was measured with a pressure transducer through an intraventricle tube. Repeated surgical drainage was performed while ICP was controlled with barbiturate therapy. He was discharged with no neurological deficits. In patients with an extensive SDE over the cerebral hemisphere, ICP control with barbiturate therapy may enhance the therapeutic effect of surgical drainage.