Summary:Purpose: Arachnoid cysts are sometimes encountered in MRIs performed for a variety of reasons. In patients with epilepsy, particularly those with refractory epilepsy, arachnoid cysts are often assumed to be related to their seizure focus. We conducted a study to investigate this putative relationship.Methods: A retrospective study on the incidence of arachnoid cysts was performed in patients seen in our Epilepsy Clinic who had CT or MRI scans, interictal EEGs or ictal EEGS. Locations of seizure foci in these patients were defined from clinical and electrophysiologic data.Results: Seventeen of 867 patients had arachnoid cysts.Twelve patients had temporal lobe cysts and only 3 of them had temporal lobe seizures. Four patients had frontal lobe cysts and only 1 had frontal lobe seizures ipsilateral to the cyst. One patient had a cerebello-pontine angle cyst and frontal lobe seizures. Thus, clinical manifestations of seizures and EEG findings (interictal and/or ictal) indicated that the seizure focus was adjacent to the cysts in only 4 patients (23.5%).Conclusions: Our findings suggest that arachnoid cysts are often an incidental finding in patients with epilepsy and do not necessarily reflect the location of the seizure focus. Key Words: Arachnoid cysts-Frontal lobe seizures-Temporal lobe seizures-Complex partial seizures-Epilepsy surgery.Arachnoid cysts are frequently encountered in association with various neurological disorders, including epilepsy (1-3). In a recent study of 27 patients with arachnoid cysts in the middle cranial fossa, 10 had neurologic symptoms not referable to the cyst, 17 had neurologic symptoms which were possibly related to the cyst, and 7 of these 17 patients had epilepsy (3).Arachnoid cysts are congenital lesions of unknown causes and consist of a reduplication of the arachnoid membrane within which fluid collects as a cyst (4). The etiology of the cysts is controversial, but it has been ascribed to congenital malformation, infection, trauma, or increased intracranial pressure. Their most common locations in the sylvian or choroidal fissure (3). In most cases, cysts are not associated with progressive symptoms related to raised intracranial pressure, and frequently are detected incidentally, or following hemorrhagic complications due to minor trauma.A number of anecdotal reports have yielded inconsistent conclusions about the relationship of arachnoid cysts and epilepsy. A patient with Landau-Kleffner syndrome was reported to have an area of hypometabolism around an arachnoid cyst. Shunting of the cyst led to seizure Accepted May 7, 1997. Address correspondence and reprint requests to Dr. S. Arroyo at Servicio de Neurologia, Hospital Clinic i Provincial de Barcelona, cNillarroel 170, Barcelona 08036, Spain. improvement and reduction of the hypometabolism (5).However, bilateral temporal lobe cysts were described in a patient with multifocal epilepsy and Lennox-Gastaut syndrome, suggesting that arachnoid cysts in themselves are not necessarily related to a specific epileptogenic regi...
SUMMARY We studied 8 patients with cerebral infarction in the deep territory of the middle cerebral artery (MCA). All patients had a definite cardiac source of emboli and no known factors for thrombosis. Mixed sensory and motor deficit was found in all but one patient and CT scan showed larger lesions than usually reported in lacunar infarcts. Contrast enhancement was seen in all cases in which CT scan was performed in the second or third week. It is concluded that embolic infarcts in deep cerebral territory of MCA from a cardiac source are more frequent than previously reported. This diagnosis has to be consid ered when CT scan demonstrates a deep cerebral infarct.Stroke Patients and MethodsWe reviewed records of all patients with deep cere bral infarcts confirmed by CT seen during the period 1979-1981. Patients with hypertension (blood pres sure equal or more than 160/95 mm Hg in several determinations) diabetes, blood hematocrit greater than 45%, heavy cigarette smoking or vasculitis were excluded. This review yielded 8 patients without known risk factors for a thrombotic disease and with a definite heart disease with high probability of cerebral embolization. Six patients had rheumatic heart disease and mitral valve stenosis, five of them with atrial fi brillation. The disease was diagnosed by clinical histo ry and auscultation. In three cases it was confirmed at surgery. One patient had an aortic prosthetic valve (Starr-Edwards) and anticoagulation had been stopped one year before the stroke because of gastrointestinal bleeding. Another patient had a subacute bacterial en docarditis with blood cultures positive for Streptococ- cus salivarius and infected vegetations were confirmed at surgery. Results Clinical and CT findings are summarized in table 1.The clinical deficit had an abrupt onset, reaching its peak in a few minutes in half of the patients. In two patients, the deficit progressed during the next 3 hours; and in the remaining 2, a fluctuating course over sever al hours was seen before stabilization occurred. Neuro logical examination showed a complete (5 cases) or incomplete (3 cases) hemiplegia, accompanied by hypesthesia in 6 patients. A pure motor hemiplegia was only seen in one case. In three of them, a transitory anosognosia was clearly observed. In a further patient (case 8), the motor hemiplegia was accompanied by an expressive dysphasia. Her language disorder was char acterized by nonfluent conversational speech, naming and reading difficulties, dysgraphia and a normal audi tory comprehension. She was almost normal one year after the stroke. Recovery of the motor and sensory deficit was complete in two patients, moderate in four, and poor in two. EEG was performed on 7 patients. In all but one case, EEG showed a discrete focal slowing. The most common CT abnormality, seen in four cases, was a well-defined low density area placed in caudate, putamen and anterior limb of internal capsule ( fig. 1). In a further 3 cases, CT showed a posterior extension (fig. 2). The patient with aphasia had...
More than a half of TS females presented HL. SNHL is the most frequent pattern among middle-aged women with TS. Old age, karyotype and recurrent otitis are predisposition factors to produce HL, while oestrogens play a minor role.
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