The incidence of intracranial hemorrhage (0.1%) and fatal bleeding (0.2%) were the same in both groups. Other bleeding events that were reported more frequently in the clopidogrel group were epistaxis, hematuria, and bruise.
The overall incidence of bleeding is described in Table 1.
Table 1: CURE Incidence of Bleeding Complications (% patients) Event Plavix
(+ aspirin)* Placebo
(+ aspirin)* p-value
(n=6259) (n=6303)
*
Other standard therapies were used as appropriate.
There is no edema, mass effect, or midline shift. There is no intracranial hemorrhage or evidence to indicate acute infarction.
The sella is normal. The brain stem, posterior fossa and upper cervical cord are unremarkable.
Dural venous sinuses and the major intracranial vessels show normal T2 signal void.
The mastoid air cells, visualized paranasal sinuses and orbits are normal.
The calvarium and visualized cervical vertebrae show normal marrow signal.
Idiopathic IH is in general not considered to cause increased risk of mortality. Spontaneous hemorrhage in IH is rare, and while hemorrhage in patients with IH can occur as a complication of lumbar puncture, this is rare as well. Herniation is also very rare if the IH is really idiopathic, if there are no associated brain abnormalities; the risk of herniation following lumbar puncture is less than 1%.
“Generally, the relative frequency of vascular malformations as a cause of intracranial hemorrhage is approximately 5%. In particular, the risk of hemorrhage of cavernous angiomas is estimated to be less than 2% per lesion per year. As a cause of hemorrhage, cavernous angiomas are far less common than hypertension; nevertheless, as a cause of hemorrhage, they must be excluded, especially in young patients.
Unfortunately, if you have encountered an injury, followed by headache, you need to report to the emergency room immediately along with an attendant due to risk of symptoms worsening rapidly. There is a risk of concussion. intracranial hemorrhage compressing the rest of the brain and raised intracranial pressure. You will need to undergo an urgent CT/MRI to locate any hemorrhage/hematoma.
No areas of pathological gadolinium enhancement are identified. There are no findings for acute territorial infarction or intracranial hemorrhage.
END OF IMPRESSION:
INDICATION: Visual field defect, and visual blurring in the right eye. The patient is a 54-year-old female.
TECHNIQUE: Dedicated 1.5 Tesla magnet multiplanar/multisequence MRI examination of the brain was performed.
CONTRAST: 9.6 mL of Gadavist was administered intravenously.
COMPARISON: None.
No areas of pathological gadolinium enhancement are identified. There are no findings for acute territorial infarction or intracranial hemorrhage.
END OF IMPRESSION:
INDICATION: Visual field defect, and visual blurring in the right eye. The patient is a 54-year-old female.
TECHNIQUE: Dedicated 1.5 Tesla magnet multiplanar/multisequence MRI examination of the brain was performed.
CONTRAST: 9.6 mL of Gadavist was administered intravenously.
COMPARISON: None.
No areas of pathological gadolinium enhancement are identified. There are no findings for acute territorial infarction or intracranial hemorrhage.
END OF IMPRESSION:
INDICATION: Visual field defect, and visual blurring in the right eye. The patient is a 54-year-old female.
TECHNIQUE: Dedicated 1.5 Tesla magnet multiplanar/multisequence MRI examination of the brain was performed.
CONTRAST: 9.6 mL of Gadavist was administered intravenously.
COMPARISON: None.
That report is unremarkable aka normal. Please note that CT is usually just the initial test, intended to rule out obvious mass, stroke, hemorrhage, etc. If your symptoms persist, you should follow up with your doctor to discuss if you might benefit from any other lab and/or imaging tests, including but not limited to MRI brain with and without contrast.
I had a CT scan which showed no evidence of intracranial hemorrhage, acute stroke or intracranial mass legion. The CT did show mild white matter loss in the supratentorial brain. The soonest I'm able to get an appointment with a neurologist is in two weeks. I'm worried that I could have an unruptured aneurysm and am especially concerned because my aunt died of an aneurysm when she was 35. Wondering if I should go the ER and ask for an MRI or MRA or just wait until my appointment.
I have have had issue in pass with dizzy and week and almost passing out. I have had leg cramps like in front and back of leg or in door off and in I. Pass that wakes me up in middle of night and hurts so bad will bring me to tears will try and walk it out or take hot bath. And next day will be sore. But happen more now . And after blanking out and falling and shaking will be really tired. For about a day. My husband said when a sleep I will jerk like arm or legs in my sleep.
Negative for acute intracranial hemorrhage, other intra-/extra-axial fluid collection, mass effect/midline shift, or acute osseous abnormality. Ventricular, subarachnoid, and cisternal spaces, as well as gray/white matter differentiation, appear unremarkable, within the limits of this study.
Trace scattered paranasal sinus mucosal thickening is most notable within the ethmoid sinus. The left mastoid air cell complex is moderately/severely hypoplastic.
The corpus callosum is normal in morphology and signal. The cerebellum and brainstem are norman in strcture and signal. No evidence of cortical infarct, intracranial hemorrhage, edema, mass lesion, abnormal, enhancement, or abnormal extraaxial fluid collection. The ventricles are normal and at midline. The paranasal sinuses and the arterial flow voids are patent. No chiari malformation.
)
Few (less than five) punctate areas of abnormal T2 prolongation in the subcortical white matter of the left frontal lobe and left external capsule without restricted diffusion or hemorrhage. Remainder of the study is unremarkable without an intracranial mass, mass effect or midline shift. No evidence of hydrocephalus. No intracranial hemorrhage or extraaxial fluid collection.
With large hemorrhages, especially in patients with hypertension or an underlying vascular malformation, there may be a rapid progression to coma. Intracranial hemorrhage is an important cause of acute neurologic dysfunction and accurate early diagnosis of cortical versus brainstem hemorrhage, with initiation of appropriate therapy, may help to minimize morbidity”. Taken from http://www.medlink.com/medlinkcontent.
There is no acute territorial infarction or intracranial hemorrhage. There is no mass, mass-effect or midline shift. There is mild prominence of the sulci and ventricles, constistent with age appropriate celebral atrophy. There are multiple foci of signal hyperintensity seen on T2 and FLAIR sequences within the subcortical white matter. There is no associated enhancement of these lesions. These are non specific but probably reflect microangiopathic ischemic changes. There is no hydrocephalus.
Had a CT scan on April 11th and was told no evidence of intracranial hemorrhage, mass effect, or acute major vascular territorial infarct. Diffuse white matter hypodensity in both cerebral hemispheres is nonspecific but may represent chronic microvascular change in this age group. On June 29th I had an MRI which said: 1. No evidence of acute or chronic intracranial hemorrge, masses or mass effect. No abnormal parechymal or leptomeningeal enchancement. 2.
Coreg 25 mg x 2
Lipitor 20 mg x 1
Spironolactone 25 mg x 1
Aspirin 81 mg x 1
Amitriptyline 25 mg x 1
Calcium 630 mg x 2
Vitamin D 1000 IU x 2
Glucosamine 1500 mg x 1
Chondroitin 1200 mg x 1
Four days ago she suffered a cerebral thrombosis affecting her speech center, was given t-PA, and recovered. Plavix (75 mg once per day) was added to her drug regimen Mirtazapine (7.
You need to be checked for migraines and any intracranial space-occupying lesion like a tumor, cyst or hemorrhage for this burning sensation in head. Depression can cause perception problems but an MRI head would rule out doubts. Consult a neurologist immediately. Hope this helps. Take care.
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