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Biomedical subjects

C A Sila

Publications and source records attributed to C A Sila.

17 recordsLinked to original sources

Progressive vision loss. A rare manifestation of familial cavernous angiomas.

We studied four generations of a family in which the index case had progressive loss of vision secondary to a cavernous angioma of the optic nerve and chiasm. Magnetic resonance imaging of the brain revealed multiple, asymptomatic intracerebral cavernous angiomas. Brain magnetic resonance imaging scans of the family members revealed multiple cavernous angiomas in the brother and paternal grandfather, but none in the father or his siblings. Autopsy reports of the paternal great grandfather noted multiple cavernous angiomas in the brain and abdominal viscera. We believe our patient to be the sixth reported case in which a cavernous angioma involved the optic chiasm and optic nerve. Magnetic resonance imaging is a sensitive and specific method of detecting cavernous angiomas. Cavernous angiomas have an autosomal dominant pattern of inheritance with variable penetrance. Surgical intervention in patients with symptomatic cavernous angiomas depends on the location and size of the lesion and associated surgical risks.

Adolescent

Neurologic complications related to cardiac surgery.

Neurologic complications are a major cause of morbidity, complicating open heart surgery, cardiac catheterization, and interventional techniques. Global or focal brain ischemia related to embolism or hypoperfusion predominates. Breakthrough cerebral hemorrhage and infection can complicate cardiac transplantation. Identifying individuals at risk for cerebrovascular complications may lead to more effective preventative and treatment measures.

Brain Damage, Chronic

Etiology of motor or sensory stroke: a prospective study of the predictive value of clinical and radiological features.

The diagnostic utility of clinical and radiological features for distinguishing penetrating artery disease from other causes of stroke has been questioned. To address this issue, we prospectively evaluated more than 40 features in 85 patients with pure motor, sensorimotor, or pure sensory syndromes. Nonischemic causes were present in 4 patients. The causes of ischemic stroke in the other 81 patients were penetrating artery disease (32 patients), large artery occlusive disease (17), cardioembolism (12), other causes (8), and undetermined (12). Of the features evaluated, frequent transient ischemic attacks (greater than or equal to 1/day), transient ischemic attacks occurring only within 1 week of stroke, pure motor hemiparesis (similar involvement of face, arm, and leg), pure sensory stroke, and round or oval infarction were associated (p less than 0.05) with penetrating artery disease. However, only pure sensory stroke involving two or more regions of the body and pure motor hemiparesis associated with subcortical infarction of less than 1.5 cm had positive predictive values exceeding 90% for penetrating artery disease. Carotid bruit ipsilateral to an anterior circulation infarction, monoparesis, and striatocapsular infarction had positive predictive values exceeding 90% for causes other than penetrating artery disease; however, half of the striatocapsular infarctions were of undetermined cause. These data suggest that certain clinical and radiological features are useful for distinguishing penetrating artery disease from other causes of stroke.

Aged

Reversal of a dense, persistent, holohemispheric neurological deficit after an endarterectomy of the carotid artery: case report.

The role and timing of a carotid endarterectomy in the setting of an acute ischemic stroke-in-evolution remain controversial. Although computed tomographic (CT) scans typically show no abnormalities in the acute stage, it is generally agreed that a dense neurological deficit (hemiplegia) and/or multiple modality neurological disturbance (involving motor, sensory, gaze, and visual field impairment) represent contraindications to surgical intervention. We present a case of an acute right holohemispheric neurological deficit including dense hemiplegia, hemisensory loss, gaze disturbance, hemineglect, and impaired level of consciousness. This persisted for 4 days while serial CT scans showed no evidence of infarction. Angiography revealed pre-occlusive stenosis of the right internal carotid artery with sluggish antegrade flow. The anterior collaterals of the circle of Willis were impaired, and the right middle cerebral artery territory filled via the posterior communicating artery. Despite the dense neurological deficit persisting for 4 days, a carotid endarterectomy was performed. Gradual neurological improvement was noted within hours of the operation, and all neurological deficits resolved within the subsequent 3 days. This case is consistent with prolonged holohemispheric hemodynamic compromise below the threshold of neurological dysfunction, but above the threshold of tissue infarction ("idling neurons"). Features assisting in the recognition of this unusual scenario and the indications and risks of revascularization in this setting are discussed.

Aged

Intracranial hypertension associated with unruptured cerebral arteriovenous malformations.

Only 6 patients with intracranial hypertension associated with unruptured cerebral arteriovenous malformations have been reported. We report 6 additional patients seen at the Cleveland Clinic during the past 10 years. The average age was 28 years (range, 19-44 years); 4 were women. Symptoms and signs included papilledema (6 patients), headache (6), transient nonepileptic focal symptoms (4), visual obscurations (3), ipsilateral carotid or ocular bruits (3), abnormal visual fields (3), focal seizures (2), and progressive visual loss (1). Enhanced computed tomography (CT) or magnetic resonance imaging (MRI) demonstrated the malformations in all 6 patients. The malformations were large, supplied by the branches of the middle and anterior cerebral arteries, with the posterior cerebral artery contributing in 3 patients, and all drained into the superior sagittal sinus. Associated venous obstruction was seen in 2 patients. Four patients underwent excision of the arteriovenous malformation, with resolution of papilledema in all 4. Measurements of cortical arterial and venous pressures during surgery in 3 patients showed decreased feeding artery pressures and elevated draining vein pressures, which normalized after removal of the malformation. Treatment in the 2 remaining patients consisted of medical therapy (acetazolamide, furosemide, steroids) alone in 1 patient, and in conjunction with proton beam radiation in the other. Papilledema resolved in the former patient, but the patient receiving proton beam radiation still had papilledema 2 years later. Intracranial hypertension associated with unruptured cerebral arteriovenous malformations occurs in young patients with high flow malformations that drain into the superior sagittal sinus, and is likely the result of increased cortical venous and superior sagittal sinus pressure. Excision of the malformation effectively reduces the intracranial pressure.

Adult

Mechanism of stroke in patients taking aspirin.

During a 1-year period, we prospectively studied the mechanism and severity of stroke in 47 patients sustaining a cerebral infarction while taking aspirin. The mechanism of stroke was undetermined in 12 patients (26%). In the remaining 35 patients, we identified 39 potential mechanisms: large-artery atherosclerosis (19 patients, 40%), cardioembolism (15 patients, 32%), and small-vessel occlusive disease (5 patients, 11%). Of 11 patients with carotid atherosclerosis and stroke, 9 (82%) had greater than 90% carotid stenosis or occlusion; of 12 patients with stroke of undetermined mechanism, 10 (83%) had previous stroke, of which 8 were also of undetermined mechanisms. Disability after stroke was moderate or severe in 27 patients (57%). These data suggest that (1) stroke in patients taking aspirin has a variety of etiologies and frequently causes moderate or severe disability; (2) patients with carotid disease failing aspirin often have high-grade carotid stenosis or occlusion; (3) stroke of undetermined mechanism may recur more frequently than other stroke subtypes in patients taking aspirin.

Adult

The effect of subarachnoid hemorrhage on blood and CSF atrial natriuretic factor.

Atrial natriuretic factor (ANF) is a diuretic natriuretic peptide hormone produced by both the heart and brain which has been postulated to play a role in the hemodynamic and sodium instability that frequently follows subarachnoid hemorrhage (SAH). Levels of ANF were measured in 12 patients with nontraumatic SAH and nine control patients with unruptured cerebral aneurysms. At surgery, the mean plasma ANF level (+/- standard deviation) of the SAH group was significantly higher than that of the control group (158.1 +/- 83.8 vs. 57.8 +/- 45.3 pg/ml, respectively; p = 0.01). There was no significant difference in serum sodium concentration, blood pressure, or central venous pressure between these groups. Nine patients with SAH due to aneurysm rupture had plasma ANF levels similar to those in three patients with SAH due to other causes. Four patients with moderate to severe SAH had significantly higher mean cerebrospinal fluid (CSF) ANF values (17.7 +/- 12.8 pg/ml) than five patients with minimal SAH (0.6 +/- 0.9 pg/ml) or the control group of nine patients (3.7 +/- 1.3 pg/ml) (p less than 0.05). Five patients with moderate to severe SAH had significantly higher plasma ANF values (202.6 +/- 72.2 pg/ml) than five with minimal SAH (86.8 +/- 29.2 pg/ml) or the control group (57.8 +/- 45.3 pg/ml) (p less than 0.05). Plasma ANF values were substantially higher than CSF ANF content in the SAH group (p less than 0.01) and in the control group (p = 0.05). From these data it is concluded that: 1) plasma ANF is elevated significantly after SAH; 2) this rise appears unrelated to the cause of hemorrhage, serum sodium concentration, blood pressure, or central venous pressure, but is related to the extent of the hemorrhage; 3) ANF concentrations in the CSF are significantly lower than in plasma, and are elevated after moderate to severe SAH; and 4) the source of CSF ANF is probably the plasma, and the source of plasma ANF is likely the heart.

Adult

Giant and multiple aneurysms of the distal posterior inferior cerebellar artery.

A case involving giant and multiple aneurysms of the distal posterior inferior cerebellar artery (PICA) is presented. Of the 130 reported cases of peripheral aneurysms of the PICA, 6 have been described as giant aneurysms and 5 have involved multiple aneurysms located on a single PICA. The occurrence of multiple aneurysms including one giant aneurysm has not been reported previously. A clinical description of our case as well as a review of the literature is presented.

Cerebellum

Drug treatment of stroke. Current status and future prospects.

Despite advances in the understanding of the mechanism of cerebral injury during focal ischaemia, the best treatment of cerebral ischaemia is still prevention. The pathophysiological mechanisms that contribute to cerebral ischaemia are discussed relative to the many therapeutic interventions that have been attempted. It is our impression that the treatment of such a complex multifactor process will require multimodal therapy, as most of the unifactorial therapies used to date have proven relatively unsuccessful in improving neurological outcome and survival.

Cardiovascular Agents

Pulsatile tinnitus.

Pulse-synchronous tinnitus suggests a vascular etiology and is deemed rare by the otologic literature. During the period 1978-1985 we evaluated 20 patients with the sole or initial complaint of pulsatile tinnitus. Fourteen patients had objective pulsatile tinnitus, perceived by the patient and the examiner alike, and 6 had subjective pulsatile tinnitus, perceived by the patient only. Angiographic findings in patients with objective pulsatile tinnitus included dural or pial arteriovenous malformations, occlusive disease of the intra- or extracranial carotid arteries from atherosclerosis or dissection, panarterial ectasia, and venous sinus thrombosis. Most of the patients with subjective pulsatile tinnitus had normal evaluations, but other possible causes of subjective pulsatile tinnitus included a carotid occlusion and pseudotumor cerebri. Pulsatile tinnitus is an uncommon symptom produced by a variety of causes. Given the abnormalities present in our series, we would recommend intraarterial digital subtraction angiography or conventional angiography in the evaluation of objective pulsatile tinnitus and intravenous digital subtraction angiography for subjective pulsatile tinnitus. Increased intracranial pressure must also be considered.

Adult

Stereotactic biopsy of non-neoplastic lesions in adults.

Stereotactic biopsy of intracranial lesions has been used primarily for the diagnosis of neoplastic lesions. A series of 158 consecutive stereotactic biopsies performed at The Cleveland Clinic Foundation resulted in 28 diagnoses of non-neoplastic disorders (18%). The majority of these were infectious, inflammatory, or demyelinating disorders. Stereotactic biopsy alone was diagnostic in 17 cases (61%), and biopsy in conjunction with clinical and laboratory data established definitive diagnoses in six cases (22%). All 23 definitive diagnoses led to modifications in patient management. Permanent neurologic morbidity occurred in only two patients (7%). We maintain that this procedure is underused. Stereotactic biopsy is safe, accurate, and useful for diagnosis of non-neoplastic neurologic disorders when the diagnosis is unclear by conventional means. In such cases, its use can lead to early diagnosis and treatment.

Adult