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.     

Contralateral mesencephalic injury due to tentorial uncal herniation. Magnetic resonance imaging of the Kernohan's notch

We report a case of a traumatic epidural hematoma with ipsilateral hemiparesis, due to the so-called Kernohan's notch. We document the injury with axial and coronal magnetic resonance imaging.     

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.     

What is causing crescendo transient ischemic attacks?

BACKGROUND AND METHODS: We discuss a case report from a patient who had symptoms of transient neurological deficits in the presence of a chronic subdural hematoma and severe carotid stenosis. Multi-modality imaging was used to guide management. RESULTS: The symptoms settled without carotid intervention and were presumed due to the subdural hematoma. CONCLUSIONS: Severe symptomatic carotid stenosis is treated with carotid endarterectomy. In some patients with transient neurological deficits, the diagnosis is not as simple as first thought. Multi-modality imaging (MRI, TCD and CT) can help differentiate the causative lesion.     

Kernohan's notch phenomenon demonstrated by diffusion tensor imaging and transcranial magnetic stimulation

Kernohan's notch phenomenon is the ipsilateral hemiplegia caused by compression of the contralateral cerebral peduncle against the tentorial edge by a supratentorial mass. Diffusion tensor imaging (DTI) and transcranial magnetic stimulation (TMS) could be useful for exploring the state of the corticospinal tract (CST). This report attempts to demonstrate Kernohan's notch phenomenon in a patient with subdural haematoma by using DTI and TMS. One patient and six normal control subjects were recruited. The patient showed severe right hemiplegia even though the subdural haematoma was located in the right hemisphere. Brain CT at the time of onset showed right transtentorial herniation, and T2 weighted images at 6 weeks after onset showed a leucomalacic lesion on the left cerebral peduncle. DTI and TMS were performed at 6 weeks after onset. The fractional anisotrophy value of the left midbrain and medulla of the patient was found to be decreased in comparison with that of the control subjects. On fibre tractography for the CST, an interruption was observed in the left midbrain and medulla. The motor evoked potential obtained from the right hand muscle showed delayed latency, low amplitude and a higher excitatory threshold, thus indicating that the CST of the left hemisphere had been damaged. It seems that the CST had been damaged at the left midbrain, although subdural haematoma and transtentorial herniation had occurred in the right hemisphere in this patient. This report demonstrates Kernohan's notch phenomenon in this patient using DTI and TMS.     

Infected subdural hematoma

A case is presented in which Escherichia coli seeded a pre-existing chronic subdural hematoma. A 77-year-old woman was admitted to our hospital because of lethargy, left hemiparesis and fever. Drainage through a burr hole was performed with the diagnosis of bilateral chronic subdural hematoma. Operative findings revealed the infected subdural hematoma on the right side and non-infected subdural hematoma on the left side. Cultures of the subdural hematoma grew Escherichia coli. In view of the pyuria, the etiology of the infected subdural hematoma was postulated to be a urinary tract infection. In the majority of 14 reported cases, the causative organisms were Escherichia coli, Salmonella, and the systemic sources of infection included the urinary tract, gastrointestinal disease, or were unknown. The possibility of infected subdural hematoma should be considered when computed tomography findings suggestive of chronic subdural hematoma exist in a patient with signs of infection.     

Armored brain in patients with hydrocephalus after shunt surgery: review of the literatures

Armored brain or chronic calcified subdural hematoma is a rare complication of cerebrospinal fluid diversion with few cases reported in the literature. Seventeen patients with this pathology have been published. A complete review of the literatures regarding this topic has been collected and discussed. The author also presents a 12- year old boy with triventricular hydrocephalus who had undergone ventriculoperitoneal medium pressure shunt system since birth. The patient presented to our clinic with a 2-year history of seizures. The patient was conscious and without neurological deficits on examination. Computed tomography of the brain showed bilateral high density mass with surface calcification. X ray skull and MRI confirmed the calcified subdural hematoma bilaterally. We preferred conservative treatment and the patient continued his antiepileptic treatment. At one year follow up, the patient had the same neurological state. The case highlights the importance of frequent follow up CT brain after shunt surgery.     

Clinical study of cerebral blood flow in bilateral chronic subdural hematoma measured by 99mTc-HMPAO SPECT]

Cerebral blood flow(CBF) in 34 patients with bilateral chronic subdural hematoma was measured by 99mTc-HMPAO SPECT before operation. The regional CBF was measured in 26 regions of the 10 cortical regions, putamen, thalamus and cerebellar hemisphere on both sides. According to the thickness of subdural hematoma, the thicker hematoma side was measured and examined as the thick hematoma side, and the other side as the thin hematoma side. Thirty four cases with bilateral chronic subdural hematoma were classified into four groups on the basis of clinical symptoms: 13 cases with headache(headache group), 10 cases with hemiparesis(hemiparesis group), 5 cases with tetraparesis(tetraparesis group) and 6 cases with consciousness disturbance or dementia(consciousness disturbance group), and into two groups according to the degree of midline brain shift on MRI: 14 cases of non-shifted group and 20 cases of shifted group. The average CBF of 34 patients in each region indicated a regional CBF reduction in the frontal, parietal and occipital cortices on the thin hematoma side, and in the putamen on the thick hematoma side. In the headache group, the regional CBF reduction on the thin hematoma side was found in the frontal, parietal and occipital cortices compared with the corresponding regions on the thick hematoma side, and in thalamus on the thick hematoma side. In the hemiparesis and tetraparesis groups, there was no statistically significant CBF reduction between the thick and thin hematoma sides. In the consciousness disturbance group, the CBF reduction in whole brain was remarkably significant. By the degree of the midline brain shift, the CBF reductions between the thick and thin hematoma sides were observed. Namely, in the shifted group, the CBF reductions were noted in the frontal, parietal and occipital cortices in the thin hematoma side, and in the putamen in the thick hematoma side. We concluded that the CBF reduction of bilateral chronic subdural hematoma was bilaterally found in the hemiparesis and tetraparesis groups, and which was finally observed in whole brain in the consciousness disturbance group.     

A case of divergence palsy associated with bilateral chronic subdural hematoma

A surgical case of bilateral chronic subdural hematoma presenting with divergence palsy is reported. A 75-year-old female was admitted to hospital for investigation of 2-week history of diplopia. The initial neurological examination demonstrated no abnormal findings except Hess chart suggesting bilateral concomitant strabismus or paresis of lateral rectus on both eyes. Because of the homonymous diplopia disappeared when the object of fixation in brought closer and the patient showed no impairment of gaze movements and following movements, the patient was diagnosed as divergence palsy and referred to the Neurosurgical Service. The physical examination revealed a 75-year-old, alert, fully oriented with diplopia at distant gaze. A computerized tomographic (CT) scan showed bilateral subdural hematoma. Emergency burrhole evacuation was performed and total amount bilateral hematoma was 220ml. Diplopia disappeared postoperatively. Hess chart examined two months after the operation shows no impairment of divergence function. This is the first reported case of divergence palsy associated with bilateral chronic subdural hematoma in CT era.     

Clinical study of cerebral blood flow in unilateral chronic subdural hematoma measured by 99mTc-HMPAO SPECT]

Cerebral blood flow (CBF) measured by 99mTc-HMPAO SPECT before operation was studied in 60 patients with unilateral chronic subdural hematoma. The regional CBF was measured in 26 regions of the fronto-occipital 10 cortices, putamen, thalamus and cerebellar hemisphere on both sides. Sixty cases with unilateral chronic subdural hematoma were classified into four groups on the basis of clinical symptoms: 17 cases with headache (headache group), 34 cases with hemiparesis (hemiparesis group) and 9 cases with consciousness disturbance or dementia (consciousness disturbance group), and into three groups on the basis of the degree of midline brain shift on MRI: 7 cases of mild shift group, 24 cases of moderate shift group and 29 cases of severe shift group. The average CBF in 60 patients in each region indicated that the regional CBF was reduced in frontal, occipital cortices and cerebellum on the non-hematoma side, and in putamen and thalamus on the hematoma side. In the headache group, the regional CBF reduction on the non-hematoma side was found in only frontal and occipital cortices compared with the corresponding regions on the hematoma side. In the hemiparesis group, the regional CBF was reduced in frontal and occipital cortices on the non-hematoma side and in putamen and thalamus on the hematoma side. The part of CBF reduction in both hemispheres was also noted in the hemiparesis group. In the consciousness disturbance group, the CBF reduction was markedly noted in whole brain. The CBF reductions in frontal and occipital cortices on the non-hematoma side and in putamen, thalamus and cerebellum on the hematoma side was not mutually related with the degree of midline brain shift. We concluded that the disturbance of CBF in chronic subdural hematoma was started from frontal and occipital cortices on the non-hematoma side observed in the headache group, and which was extended to putamen and thalamus on the hematoma side and a part of both hemispheres observed in the hemiparesis group. And such disturbance was finally observed as the CBF reductions in whole brain in the consciousness disturbance group.     

Spontaneous chronic spinal subdural hematoma associated with spinal arachnoiditis and syringomyelia

Spontaneous chronic spinal subdural hematoma is rare. We describe a case of spontaneous chronic spinal subdural hematoma associated with arachnoiditis and syringomyelia in a 76-year old woman who presented with a 14-year history of progressive myelopathy. MRI scan revealed a thoraco-lumbar subdural cystic lesion and a thoracic syrinx. The patient underwent thoracic laminectomy and decompression of the lesion, which was a subdural hematoma. A myelotomy was performed to drain the syrinx. Pathological examination revealed features consistent with chronic subdural membrane. This report attempts to elucidate the pathogenesis of chronic spinal subdural hematoma. We discuss possible etiological factors in light of the current literature and pathogenesis of both spinal subdural hematoma and syrinx formation.     

Acute Spontaneous Spinal Subdural Hematoma with Vague Symptoms

Spinal subdural hematoma is a rarely reported disease and spontaneous spinal subdural hematomas (SSDH) without underlying pathological changes are even rarer. The patients usually show typical symtoms such as back pain, quadriplegia, paraplegia or sensory change. But rarely, patients may show atypical symptoms such as hemiparesis and misdiagnosed to cerebrovascular accident. We recently experienced a case of SSDH, where the patient initially showed vague symptoms, such as the sudden onset of headache which we initially misdiagnosed as subarachnoid hemorrhage. In this case, the headache of patient improved but the neck pain persisted until hospital day 5. Therefre, we conducted the MRI of cervical spine and finally confirmed SSDH. The patient was managed conservatively and improved without recurrence. In this case report, we discuss the clinical features of SSDH with emphasis on the importance of an early diagnosis.     

A case of infected subdural hematoma following chronic subdural hematoma irrigation]

A 71-year-old female complicating Parkinson disease and diabetes mellitus was admitted to our medical center for urinary tract infection one month after burr hole irrigation and drainage of left chronic subdural hematoma. Klebsiella pneumonia was detected in the bacterial culture of her urine. As antibiotic therapy started, her condition and peripheral white blood cell counts were improved. But consciousness level got worsened and right hemiparesis appeared. A CT scan showed re-accumulation of left subdural fluid so an emergent irrigation was performed. The old hematoma with slightly yellowish, bloody purulent fluid was found and an intracapsular drain was inserted. Klebsiella pneumonia was detected from the bacterial culture of the hematoma. After 10 days, a CT scan showed subdural fluid collection again, so, total hematoma capsule removal was performed. After the operation, her neurological and serological condition improved and she was discharged without any neurological deficits. Klebsiella pneumonia existing urinary tracts rarely infected subdural hematoma cavity via hematogenous dissemination. We must keep in mind this complication may occur when we see compromised host like this case. Total removal of infected hematoma capsule is considered as radical treatment.     

Idiopathic Hypertrophic Cranial Pachymeningitis Misdiagnosed as Acute Subtentorial Hematoma

A case of idiopathic hypertrophic cranial pachymeningitis (IHCP) misdiagnosed as an acute subdural hematoma is reported. A 37-year-old male patient presented with headache following head trauma 2 weeks earlier. Computerized tomography showed a diffuse high-density lesion along the left tentorium and falx cerebri. Initial chest X-rays revealed a small mass in the right upper lobe with right lower pleural thickening, which suggested lung cancer, such as an adenoma or mediastinal metastasis. During conservative treatment under the diagnosis of a subdural hematoma, left cranial nerve palsies were developed (3rd and 6th), followed by scleritis and uveitis involving both eyes. Magnetic resonance imaging (MRI) revealed an unusual tentorium-falx enhancement on gadolinium-enhanced T1-weighted images. Non-specific chronic inflammation of the pachymeninges was noticed on histopathologic examination following an open biopsy. Systemic steroid treatment was initiated, resulting in dramatic improvement of symptoms. A follow-up brain MRI showed total resolution of the lesion 2 months after steroid treatment. IHCP should be included in the differential diagnosis of subtentorial-enhancing 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 acute traumatic subdural hematoma in a child with previous bilateral encephaloduroarteriosynangiosis

The authors report the case of a 5-year-old female with right-sided hemiparesis and aphasia secondary to moyamoya disease, who had previously undergone staged bilateral encephaloduroarteriosynangiosis procedures. A subsequent ground-level fall caused an acute traumatic subdural hematoma with mass effect and neurological decline. She underwent emergency hematoma evacuation and decompressive craniectomy, which required interruption of the superficial temporal artery that had been used for indirect bypass, followed later by autologous cranioplasty. There were no acute or long-term ischemic events related to the occurrence or treatment of the traumatic hematoma. Follow-up angiography revealed extensive spontaneous vascular collateralization in the field of the decompressive craniectomy and cranioplasty. The patient returned to her pre-injury neurological baseline.     

Cervical syringohydromyelia secondary to chronic supratentorial subdural hematoma

Introduction: Syringohydromyelia associated with supratentorial space-occupying lesion has rarely been reported. We present a 28-year-old woman was admitted to the hospital with head and neck pain. Upon examination, there was only left central facial paralisia, with no evidence of papilledema. Methods and Results: Cranial magnetic resonance imaging (MRI) revealed a left parietal and temporal chronic subdural hematoma (CSH) with a 1-cm shift to the right from midline. Also, cervical MRI revealed a syringohydromyelic cavity at the level of C6/7. The patient was operated on for supratentorial CSH. A follow-up cervical MRI revealed no syringohydromyelic cavity after 2 months. No neurological deficit was reported, and overall outcome was excellent. Conclusion: Syringohydromyelia was secondary to a space-occupying lesion in our case of supratentorial chronic subdural hematoma.     

Arachnoid cysts of the middle cranial fossa presented as subdural hematomas

The aim of the study was to present the authors' own experience and discuss the treatment method of arachnoid cysts of the middle cranial fossa disclosed as subdural hematoma. Three cases of male patients operated on because of chronic subdural hematoma are presented. Control CT studies after evacuation of hematomas revealed arachnoid cysts of the middle cranial fossa and all patients were qualified for delayed cystocisternostomy by open craniotomy. Indirect signs of presence of arachnoid cysts in the form of bony abnormalities and expanded the middle cranial fossa in the first CT were seen in all patients. Cysts were asymptomatic until the injury in all cases. The volumes of cysts in MRI scans were: 17.8 ml, 52.9 ml and 92.4 ml, respectively. All cysts were type II according to Galassi classification. After control MRI described above made to evaluate cyst appearance, delayed cystocisternostomy to basal cisterns was undertaken in two cases with full success. No complications were observed. The third patient refused surgery. During surgery the thick and non-transparent medial cyst wall and arachnoidea of tentorial notch cisterns were observed impeding the exact identification of neurovascular structures. In our opinion arachnoid cysts of the middle cranial fossa revealed as subdural hematoma should be operated on in two stages: in the first step subdural hematoma should be evacuated and in the second step cystocisternostomy should be performed. With regard to observed morphological changes of arachnoidea and cyst walls we think that open cystocisternostomy is treatment of choice in these cases.     

Subacute spinal subdural hematoma associated with intracranial subdural hematoma

We describe a subacute spinal subdural hematoma in a patient with psot-traumatic subacute intracranial subdural hematoma. CT and MRI demonstrated hematoma within the interhemispheric subdural space and at the lumbar posterior subdural space which extended from the L1 to the S2 level. The lesion showed high signal intensity on both T1 and T2 weighted images. Surgical decompression of the spinal subdural hematoma was performed. The symptoms completely resolved after surgery. Spinal subdural hematoma may be concomitant with or may occur after intracranial subdural hematoma. If a patient with intracranial subdural hematoma complains of low back pain and weakness in both legs; lumbosacral MR examination should be performed to exclude spinal subdural hematoma.     

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.