Remote cerebellar hemorrhage: A case report.
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ABSTRACT:
SUBMITTER: Omer A
PROVIDER: S-EPMC6360913 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Idiopathic intracranial hypertension is characterized by high intracranial pressure without hydrocephalus or intracranial mass. Surgical treatment includes optic nerve fenestration and insertion of ventriculoperitoneal and lumboperitoneal (LP) shunts. For decreasing intracranial pressure, cerebrospinal fluid (CSF) LP shunt is widely used for the surgical management; it also carries complications such as shunt migration, venous sinus thrombosis, subarachnoid hemorrhage, and subdural and intracerebral hematoma. A 52-year-old man was admitted to the neurosurgery clinic with severe headache, retro-orbital pain, and blurred vision. Lumbar puncture demonstrated that the CSF opening pressure was 32 cm H 2 O. A nonprogrammable LP shunt with two distal slit valves was inserted. Shortly after the surgery, his condition deteriorated and he became comatose. Immediate computed tomography scan revealed cerebellar hemorrhage and acute hydrocephalus. Development of remote cerebellar hemorrhage following LP shunt is rare. We discuss this rare event and the applicable literature.
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Project description:Background Cerebellar glioblastoma multiforme (GBM) is rare and presents with increased intracranial pressure and cerebellar signs. The recommended treatment is radical resection, if possible, with radiation and chemotherapy. Clinical Presentation A 53-year-old man presented with hypertensive cerebellar bleeding and a 2-day history of severe headaches, nausea, vomiting, gait instability, and elevated blood pressure. Computed tomography (CT) showed a left cerebellar hematoma with no obstruction of cerebrospinal fluid and no hydrocephalus. CT angiography showed no signs of pathologic blood vessels in the posterior cranial fossa. The patient was observed in the hospital and discharged. Subsequent CT showed complete hematoma resorption. Two weeks later, he developed headaches, nausea, and worsening cerebellar symptoms. Magnetic resonance imaging (MRI) showed a 4-cm diameter tumor in the left cerebellar hemisphere where the hemorrhage was located. The tumor was radically resected and diagnosed as GBM. The patient underwent radiation and chemotherapy. At a follow-up of 1.5 years, MRIs showed no tumor recurrence. Conclusion Hypertensive cerebellar hemorrhage may be the first presentation of underlying tumor, specifically GBM. Patients undergoing surgery for cerebellar hemorrhage should have clot specimens sent for histologic examination and have pre- and postcontrast MRIs. Patients not undergoing surgery should have MRIs done after hematoma resolution to rule out underlying tumor.
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Project description:BackgroundDiaphragmatic myoclonus is a rare motor disorder that affects muscle tone. It is characterized by involuntary movements of the abdominal wall and rhythmic, repetitive contractions of the accessory or respiratory muscles, all of which are innervated by the cervical nerve roots.Case descriptionWe reviewed the case of a 57-year-old male patient who underwent surgery for a left cerebellar hemorrhage. He exhibited persistent myoclonus in the palate, jaw, and thoracoabdominal region. Following treatment, there was a significant reduction in flutter amplitude in these areas.ConclusionThe clinical rarity and variability of presentations often make diagnosis challenging and delayed. It is believed that this condition stems from abnormal excitation within the central nervous system or neural pathways that involve the phrenic nerve. Another potential mechanism is the direct irritation of the diaphragm. Ultrasound, chest fluoroscopy, and electromyography (EMG) can support the diagnosis. Various pharmacological and surgical treatments have been tried, yet specific treatment guidelines are still lacking.
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Project description:Study Design Case report. Objective To report a case of remote cerebellar hemorrhage (RCH) without intraoperative dural tear after revision lumbar spine surgery. RCH is a rare postoperative complication following spine surgery. RCH has previously been reported only in cases with intraoperative dural tear or durotomy. Methods Case report and literature review. Results A 58-year-old woman underwent removal of L4-S1 posterior spinal instrumented fusion (PSIF) implants and L3-L4 decompressive laminectomy with PSIF. There was no intraoperative dural tear. After doing well initially, the patient developed new neurologic symptoms and was found to have RCH. Lumbar spine magnetic resonance imaging (MRI) demonstrated a large dural defect. After repair of the dura, the patient had dramatic improvement of her neurologic symptoms. At 1-year follow-up, the patient continued to have no neurologic sequelae. Conclusion This report demonstrates that RCH can occur without intraoperative dural tear. Although rare, any patient with new onset of declining neurologic symptoms following spine surgery should have a brain MRI and should have RCH on the differential diagnosis.
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Project description:ACTA2 encodes smooth muscle specific ?-actin, a critical component or the contractile complex of vascular smooth muscle. Mutations in ACTA2 are the most common genetic cause of thoracic aortic aneurysm, and are also the cause of other disorders, including Moyamoya disease, coronary artery disease and stroke as well as Multisystemic Smooth Muscle Dysfunction Syndrome. We note that ACTA2 is also expressed in uterine smooth muscle, and this raises the possibility that women harboring ACTA2 mutations might exhibit uterine smooth muscle dysfunction.We present a young woman whose ACTA2 mutation was ascertained during pregnancy because of her father's history of dissecting aneurysms. She was delivered at full term by cesarean section and subsequently had severe uterine hemorrhage due to uterine atony. Although her atony was successfully treated with uterotonic medications, she required blood transfusion.This case raises the possibility that women with ACTA2 mutations may be at risk of uterine muscle dysfunction and hemorrhage. Obstetricians should be alerted to and prepared for this possibility.
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Project description:BackgroundDense exudate during the calcification of cerebral cysticercosis in basal subarachnoid space was easy to be misdiagnosed as subarachnoid hemorrhage (SAH); clinical evaluation and MRI can help differentiate SAH from pseudo-SAH.Case presentationA case of ventricular expansion accompanied by high-density shadows in cisterna circinata cerebri was taken to the hospital for treatment due to sudden faint. This patient was diagnosed as subarachnoid hemorrhage according to computed tomography (CT) in another hospital. We believe that the high density in cisterna circinata cerebri was misdiagnosed as subarachnoid hemorrhage (SAH) 1 year ago. The main etiology of SAH is aneurysm; non-aneurysmal SAH associated with cerebral cysticercosis is extremely rare. Only 5 patients have been reported.ConclusionThis case indicated that although the specificity of CT for SAH is very high, the physicians should be aware of rare false positive findings, called pseudo-SAH.
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Project description:BackgroundSuperior vermian subtype of arteriovenous malformation (AVM) coexisting with proximal feeder aneurysm on basilar-superior cerebellar artery (BA-SCA) junction is an extremely rare situation. We experienced a case of this rare entity presenting with subarachnoid hemorrhage (SAH), and herein, introduce the outline and clinical features of this experience together with the actual surgical video.Case descriptionA 54-year-old man SAH patient with severe headache, disturbance of consciousness, and left oculomotor palsy was urgently admitted to our hospital. Imaging examination demonstrated superior vermian AVM with BA-SCA aneurysm, and both lesions were treated through two different approaches (left pterional craniotomy in conjunction with zygomectomy, and left posterior interhemispheric occipital transtentorial approach) in acute phase of SAH. Both lesions were completely disappeared postoperatively and the patient's postoperative course was favorable, without symptomatic cerebral vasospasm. Although slight oculomotor palsy remained, the patient recovered well and was transferred to a rehabilitation hospital for further improvement.ConclusionIn the cases of AVM coexisting with proximal feeder aneurysm, presenting with SAH, disorders of intracranial venous return associated with an AVM can be a vital hindrance to managing cerebral vasospasm; therefore, treating both lesions in the acute phase may lead to good outcomes.
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