Cases reported "Vasospasm, Intracranial"

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1/92. Very late-onset symptomatic cerebral vasospasm caused by a large residual aneurysmal subarachnoid hematoma--case report.

    A 70-year-old female developed delayed ischemic neurological deficits at 35 days after subarachnoid hemorrhage (Hunt and Kosnik grade III, Fisher group 4) caused by a ruptured aneurysm of the left middle cerebral artery. Angiography indicated late-onset cerebral vasospasm probably due to the mass effect of a large hematoma remaining in the sylvian fissure and an intracerebral hematoma after surgery. patients with a large subarachnoid hematoma after subarachnoid hemorrhage should receive therapy to prevent cerebral vasospasm until the mass effect of the hematoma has diminished. ( info)

2/92. Making sense out of jargon: a neurolinguistic and computational account of jargon aphasia.

    OBJECTIVE: To identify the cognitive and neuroanatomic bases of neologistic jargon aphasia with spared comprehension and production of written words. methods: Detailed analysis of performance across experiments of naming, reading, writing, repetition, and word/picture matching by a 68-year-old woman (J.B.N.) served to identify which cognitive mechanisms underlying naming and word comprehension were impaired. J.B.N.'s impairments were then simulated by selectively "lesioning" a computer model of word production that has semantic, word form, and subword phonologic levels of representation (described by Dell in 1986). RESULTS: In comprehension experiments, J.B.N. made far more errors with spoken word input than with written word or picture input (chi-square = 40-59; df = 1; p < 0.0001) despite intact auditory discrimination. In naming experiments (with picture, definition, or tactile input), J.B.N. made far more errors in spoken output relative to written output (chi-square = 14-56; df = 1; p < 0.0001). These selective impairments of spoken word processing were simulated by reducing connection strength between word-level and subword-level phonologic units but maintaining full connection strength between word-level and semantic units in Dell's model. The simulation yielded a distribution of error types that was nearly identical to that of J.B.N., and her CT and MRI scans showed a small subarachnoid hemorrhage in the left sylvian fissure without infarct. Cerebral angiogram showed focal vasospasm in sylvian branches of the left middle cerebral artery. CONCLUSION: Focal left perisylvian dysfunction can result in a highly selective "disconnection" between word-level and subword-level phonologic representations manifest as neologistic jargon aphasia with intact understanding and production of written words. ( info)

3/92. Acute intermittent porphyria with central pontine myelinolysis and cortical laminar necrosis.

    Acute intermittent porphyria (AIP) is an autosomal-dominant disease caused by a deficiency of porphobilinogen (PBG) deaminase. patients with AIP present with neurological syndromes such as autonomic neuropathy, peripheral axonal neuropathy or central nervous system dysfunction. We report serial MRI of a patient with AIP who had cortical and subcortical cerebral changes. A 29-year-old woman with a 6-month history of AIP had an attack with severe hyponatraemia and generalised convulsions, treated with haem arginate and supportive therapy. MRI showed central pontine and extrapontine myelinolysis and cortical laminar necrosis. These are not common in AIP, but are likely to have been caused by rapid correction of hyponatraemia and by vasospasm, which could be induced by AIP. ( info)

4/92. Using transcranial Doppler sonography to augment the neurological examination after aneurysmal subarachnoid hemorrhage.

    Vasospasm is the leading cause of death in patients who survive initial subarachnoid hemorrhage (SAH). Evidence of blood in the subarachnoid space on computed tomography (CT) scan can often predict the occurrence of vasospasm. Clinically, the onset of new or worsening neurological symptoms is the most reliable indicator of vasospasm. Transcranial Doppler (TCD) sonography studies can further aid the neuroscience nurse's assessment for vasospasm by measuring cerebral blood flow velocities. Physiological changes that occur during vasospasm cause the lumen of the blood vessel to decrease, increasing blood flow velocity through the affected area. Although vasospasm can only be definitively diagnosed by cerebral angiogram, TCD sonography provides a noninvasive, low-risk assessment tool that can be done at the beside. By coupling a patient's vital neurological data with blood flow velocity trends, the neuroscience nurse can anticipate the onset or worsening of vasospasm. This advanced nursing assessment allows for collaboration with the medical team to initiate and adjust appropriate therapies to improve patient outcomes. ( info)

5/92. Use of intra-aortic balloon pump counterpulsation for refractory symptomatic vasospasm.

    Delayed neurologic deficits secondary to vasospasm remain a vexing problem. Current treatments include: hypertensive hypervolemic hemodilution (Triple-H) therapy, angioplasty, and intra-arterial papaverine administration. Significant morbidity and mortality still result from vasospasm despite these therapies. We present two patients with symptomatic vasospasm who received intra-aortic balloon pump counterpulsation (IABP) to improve cerebral blood flow when they were unable to tolerate Triple-H therapy. One patient (L.T.) developed vasospasm after resection of a meningioma that encased the carotid and middle cerebral artery. The other patient (D.F.) suffered a subarachnoid hemorrhage (Fisher Grade III, Hunt/Hess Grade III) from a basilar tip aneurysm. Postoperatively, both patients developed vasospasm. Treatment with Triple-H therapy, angioplasty, and papaverine yielded modest results. When they experienced cardiac ischemia, Triple-H therapy was stopped, but their neurologic condition deteriorated markedly. Because of this, IABP was started. Both patients had an immediate improvement in cardiac function. IABP was able to reverse some of the neurologic deficits, and was weaned off after several days of support. Both patients had a substantial improvement in function, and are now capable of caring for themselves. We conclude that IABP may play an important role for improving cerebral blood flow in patients with vasospasm. It may be particularly useful in those patients with limited cardiac reserve. ( info)

6/92. Diffuse vasospasm after pretruncal nonaneurysmal subarachnoid hemorrhage.

    Pretruncal (perimesencephalic) nonaneurysmal hemorrhage is a benign form of subarachnoid hemorrhage (SAH). Angiographic changes of vasospasm are uncommon in patients with this type of hemorrhage, and if vasospasm is present, it is mild and focal. We report two patients with pretruncal nonaneurysmal SAH who developed severe and diffuse vasospasm, expanding the clinical spectrum of this type of SAH. The first patient was a 40-year-old woman who suffered pretruncal nonaneurysmal SAH. Angiography performed on the seventh day post hemorrhage showed diffuse and severe vasospasm affecting both the anterior and the posterior circulation. The patient was treated with hypervolemia, and she remained asymptomatic. Follow-up angiography showed resolution of the vasospasm. The second patient was a 67-year-old woman who suffered pretruncal nonaneurysmal SAH. The results of the initial angiography were normal. Repeat angiography on the ninth day post hemorrhage showed severe vasospasm in the anterior circulation and moderate vasospasm in the posterior circulation. Nine hours later, the patient developed transient dysphasia, and she was treated with hypervolemia. Three days later, a transcranial Doppler examination showed normalization of blood velocities. The presence of diffuse and severe vasospasm does not exclude a diagnosis of pretruncal nonaneurysmal SAH. ( info)

7/92. apoptosis of endothelial cells in vessels affected by cerebral vasospasm.

    BACKGROUND: Cerebral vasospasm after subarachnoid hemorrhage is a prolonged contraction that leads to cerebral ischemia or infarction. Morphological studies of cerebral arteries during vasospasm have shown extensive necrosis of smooth-muscle cells and desquamation and dystrophy of endothelial cells. The mechanism of cellular death is unknown. methods: We report an observation of apoptotic changes in the cerebral arteries of a patient who died after suffering severe cerebral vasospasm caused by aneurysmal rupture. subarachnoid hemorrhage and cerebral vasospasm were confirmed by computed tomography scanning and angiogram. Histological and immunohistological examinations for apoptosis were performed in cerebral arteries. For control, the arteries from another patient, who died of trauma without head injury, were used. RESULTS: Corrugation of the internal elastic lamina and increased amounts of connective tissue was demonstrated by light microscopy. Apoptotic changes, characterized by condensation of chromatin of the nucleus and detachment from the basal membrane, were found on transmission electron microscopy in endothelial cells. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling reaction revealed positive staining of the nuclei of the endothelial cells. CONCLUSIONS: This study demonstrates that apoptosis occurred in the cerebral arteries in a patient who died of cerebral vasospasm. The possible role of apoptosis in cerebral vasospasm is discussed. ( info)

8/92. Complications associated with intraarterial administration of papaverine for vasospasm following subarachnoid hemorrhage--two case reports.

    Complications associated with intraarterial papaverine infusion occurred in two patients treated for vasospasm due to subarachnoid hemorrhage (SAH). A 42-year-old male with an anterior communicating artery aneurysm underwent craniotomy and aneurysm clipping. Five days after the SAH occurred, angiography demonstrated moderate vasospasm in spite of hypervolemic-hypertensive therapy. During papaverine infusion into the carotid artery, he suffered loss of consciousness due to a seizure for a few minutes. A 61-year-old female with a right internal carotid-posterior communicating artery aneurysm underwent clipping. Six days after the SAH occurred, angiography demonstrated severe vasospasm in spite of hypervolemic-hypertensive therapy. Angiography performed immediately after papaverine infusion into the carotid artery revealed exacerbation of the vasospasm. Finally she suffered cerebral infarction and died. Complications of intraarterial papaverine infusion are potentially dangerous. We recommend trial administration of papaverine with angiography and neurological examination before full dose infusion to avoid complications. ( info)

9/92. basilar artery vasospasm in postpartum cerebral angiopathy.

    The reason cerebral edema in postpartum cerebral angiopathy (PPCA) occurs preferentially in the posterior brain is poorly understood. The authors present two patients with PPCA who showed vasospasm occurring earlier and more severely in the basilar artery than in the middle cerebral artery. Our patients demonstrate the difference in vascular change between the anterior and posterior cerebral vessels, explaining the susceptibility of the posterior brain to PPCA. ( info)

10/92. hellp syndrome with haemaglobin vasospasm.

    The syndrome of haemolysis, elevated liver enzymes and low platelets (hellp syndrome) is a life threatening, severe complication of pre-eclampsia with typical laboratory findings. An unusual case of a 36-year-old woman with hellp syndrome and the initial complication of intracerebral haemorrhage is presented. The diagnosis of hellp syndrome was confirmed by elevated liver enzymes, low platelets, increased total bilirubin and increased lactate dehydrogenase. The intracranial haematoma was removed with good neurological recovery ensuing. However, this case was complicated by cerebral vasospasm on the eleventh day, confirmed by cerebral angiography and computer tomographic findings. The patient died from brain swelling. Possible vasospam should be considered during the treatment of patients with hellp syndrome. ( info)
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