1/28. Falcotentorial plasmacytoma. Case report.Intracranial solitary plasmacytomas are extremely rare tumors and are often misdiagnosed preoperatively. The authors report the successful treatment of a patient who harbored such a tumor involving both the falx and tentorium; this is the second case reported. A 59-year-old woman suffered from a seizure disorder due to a falcotentorial lesion, which had been identified 3 years earlier and was thought at the time to be an en plaque meningioma. Most recently, the patient presented with symptoms of increased intracranial pressure and hemiparesis. Computerized tomography and magnetic resonance imaging of her head revealed progressive growth of the tumor. The patient underwent partial resection of the tumor and chemo- and radiation therapies. Intracranial plasmacytomas must always be included in a differential diagnosis because potential complete cure can be achieved using fairly conservative treatment modalities.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
2/28. Bilateral chronic subdural hematomas resulting in unilateral oculomotor nerve paresis and brain stem symptoms after operation--case report.An 85-year-old male presented with bilateral chronic subdural hematomas (CSDHs) resulting in unilateral oculomotor nerve paresis and brainstem symptoms immediately after removal of both hematomas in a single operation. Initial computed tomography on admission demonstrated marked thick bilateral hematomas buckling the brain parenchyma with a minimal midline shift. Almost simultaneous removal of the hematomas was performed with the left side was decompressed first with a time difference of at most 2 minutes. However, the patient developed right oculomotor nerve paresis, left hemiparesis, and consciousness disturbance after the operation. The relatively marked increase in pressure on the right side may have caused transient unilateral brain stem compression and herniation of unilateral medial temporal lobe during the short time between the right and left procedures. Another factor was the vulnerability of the oculomotor nerve resulting from posterior replacement of the brain stem and stretching of the oculomotor nerves as seen on sagittal magnetic resonance (MR) images. Axial MR images obtained at the same time demonstrated medial deflection of the distal oculomotor nerve after crossing the posterior cerebral artery, which indicates previous transient compression of the nerve and the brain stem. Gradual and symmetrical decompression without time lag is recommended for the treatment of huge bilateral CSDHs.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
3/28. neuroleptic malignant syndrome associated with olanzapine therapy: a case report.We present the case of a 42-year-old male with a history of schizophrenia who developed signs and symptoms consistent with neuroleptic malignant syndrome (NMS) after 3 weeks of treatment with Olanzapine. The patient presented with hyperpyrexia, tremors, labile blood pressure, and mental status changes that had progressed over the preceding 24 h. Laboratory data revealed a metabolic acidosis and an escalating creatinine phosphokinase. Olanzapine is a relatively new atypical anti-psychotic agent first introduced in November of 1996 under the trade name of zyprexa. Olanzapine differs from typical anti-psychotic agents in that it has a lower affinity for dopaminergic receptors and binds antagonistically to serotonin receptors in the nigrostriatal pathway. These unique properties result in relatively fewer extra-pyramidal symptoms when compared to traditional anti-psychotics. Because of olanzapine's favorable side-effect profile, it has quickly gained popularity in the psychiatric community. Although NMS is a recognized complication of anti-psychotic use, there has been only one case of olanzapine induced NMS reported in the literature. The POISON-INDEX system, used by toxicologists throughout the united states, does not list NMS as a potential reaction to olanzapine. The pharmacists at our institution were also unaware that NMS was a possible complication of olanzapine. We present this case to make clinicians aware of the potential for Olanzapine induced NMS.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
4/28. A case of severe hypertension caused by ACTH-independent macronodular adrenal hyperplasia.This report describes a rare case of ACTH-independent macronodular adrenal hyperplasia (AIMAH) arisen with symptomatic severe hypertension and hypokaliemia. A 55-year-old man was admitted to hospital with a clinical picture characterized by several episodes of transient ischemic attacks (TIA) and right hemiplegia, related to severe arterial hypertension. Laboratory tests showed urinary levels of catecholamines, metanephrines and vanillylmandelic acid (VMA) in normal range; high urinary free cortisol excretion, elevated serum cortisol with loss of the circadian rhythm and low ACTH plasma levels. ACTH failed to respond to CRH administration. serum cortisol levels were not modified after high doses of dexamethasone. MRI showed bilateral macronodular hyperplasia of adrenal glands, whereas pituitary-MRI did not show tumoral lesions. Therefore, ACTH-independent macronodular hyperplasia was suspected. Though obese, the patient had no typical Cushing habit, and symptomatic hypertension with hypokaliemia was the only clinical evidence for this rare kind of Cushing's syndrome. After obtaining a satisfactory control of blood pressure, the patient was successfully submitted to laparoscopic bilateral adrenalectomy and underwent complete clinical remission. The histology showed adrenal macronodular hyperplasia. During the twenty-four month follow-up, the patient had no further transient ischemic attacks or need of glucocorticoid replacement therapy and withdrew the antihypertensive drugs.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
5/28. Spontaneous thrombosis of a residual arteriovenous malformation in eloquent cortex after surgery: case report.OBJECTIVE AND IMPORTANCE: The presence of a residual arteriovenous malformation (AVM) on postoperative angiograms is typically an indication for prompt return to the operating room to complete resection, because of the risk of early hemorrhage. This approach, however, may involve risks of neurological deficits when the residual AVM is in eloquent cortex. We present a case of complete thrombosis of a residual AVM after surgery. This residual AVM tissue was located in eloquent cortex. Complete spontaneous thrombosis of residual AVMs after surgery has only rarely been reported. This phenomenon raises questions regarding the most appropriate management for residual AVMs in eloquent cortex. CLINICAL PRESENTATION: The patient was a 43-year-old, right-handed, male patient with an AVM centered in the left precentral gyrus. The patient presented with medically intractable seizures and progressive right hemiparesis. After AVM resection, angiography revealed a residual AVM with early venous drainage. angiography performed 1 week later demonstrated a persisting AVM nidus without early venous drainage. angiography performed 3 months later demonstrated complete thrombosis of the residual AVM. INTERVENTION: The patient has been monitored for more than 1 year, without additional symptoms or therapy. CONCLUSION: We continue to advocate prompt return to the operating room when postoperative angiography reveals a residual AVM with persistent shunting. When the residual AVM is in eloquent cortex and is small, with a single draining vein, however, observation of the patient (with strict blood pressure control) and repeat angiography after 1 week represent an alternative strategy that is supported by this case report. As this case demonstrates, it is possible for small residual AVMs to thrombose. This may avert the need for reoperation for residual AVMs in eloquent cortex, with the potential for neurological deficits.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
6/28. Complication of a large cranial defect. Case report.A patient with acute subdural hematoma was successfully treated with hemicraniectomy. He developed contralateral weakness 4 months after surgery which was reversed by cranioplasty. The presumptive mechanism is a gradient between atmospheric and intracranial pressure. Early cranioplasty is suggested to prevent this phenomenon.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
7/28. Delayed oedema in the pyramidal tracts remote from intracerebral missile path following gunshot injury.A 60-year-old man developed a severe left hemiparesis and central facial palsy, accompanied by somnolence and dysarthria 9 days after a gunshot wound to the right temporal region, from which he slowly recovered over 3 months. MRI disclosed bilateral oedema of the pyramidal tracts. This was interpreted as a consequence of the impact of the pressure wave caused by the bullet, after excluding an infectious or vascular cause.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
8/28. Transcranial motor evoked potential recording in a case of Kernohan's notch syndrome: case report.OBJECTIVE AND IMPORTANCE: Compression of the cerebral peduncle against the tentorial incisura contralateral to a supratentorial mass lesion, the so-called Kernohan-Woltman notch phenomenon, can be an important cause of false localizing motor signs. Here, we demonstrate a case in which clinical, radiological, and electrophysiological findings were used together to define this syndrome. CLINICAL PRESENTATION: A 21-year-old man sustained a left temporal depressed cranial fracture from a motor vehicle accident. Serial computed tomographic examinations demonstrated no evolution of hematomas or contusions, and he was managed nonsurgically with ventriculostomy for intracranial pressure control. Throughout his course in the neurosurgical intensive care unit, he displayed persistent left hemiparesis. INTERVENTION: Further radiological and electrophysiological studies were undertaken in an attempt to explain his left hemiparesis. Brain magnetic resonance imaging demonstrated T2 prolongation in the central portion of the right cerebral peduncle extending to the right internal capsule. Electrophysiological studies using transcranial electrical motor evoked potentials revealed both a marked increase in voltage threshold, as well as a reduction in the complexity of the motor evoked potential waveform on the hemiparetic left side. This contrasted to significantly lower voltage threshold as well as a highly complex motor evoked potential waveform recorded on the relatively intact contralateral side. CONCLUSION: This is the first time that clinical, radiological, and electrophysiological findings have been correlated in a case of Kernohan's notch syndrome. Compression of the contralateral cerebral peduncle against the tentorial incisura can lead to damage and ipsilateral hemiparesis. The anatomic extent of the lesion can be defined by magnetic resonance imaging and the physiological extent by electrophysiological techniques.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
9/28. Alternating hemiplegia of childhood: case report.We report the case of a 3 1/2 year old girl who had had attacks of alternating hemiplegia from the age of 6 months. Peculiar features from the etiopathogenetic angle seem to be the presence of a ring of mild stenosis of the vertebral artery on the right side, the influence of the upright posture on the onset of the attacks and perhaps also of variations in atmospheric pressure. The only drug that had some effect was flunarizine. Phenobartbital, haloperidol and nadolol had no appreciable effect.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
10/28. motor cortex stimulation for central pain following a traumatic brain injury.Central pain can occur in any lesions along the central nervous system affecting the spinothalamocortical pathway. Although diverse etiologies have been reported to cause central pain, there are few reports on the occurrence and surgical treatment of central pain following a traumatic brain injury (TBI). This paper describes the occurrence of central pain following a severe TBI, in which the diagnosis of central pain was typically delayed due to the patient's decreased ability to express his pain for severe aphasia as a neurological sequela. The severe burning pain, deep pressure-like pain, and deep mechanical allodynia, which presented over the contralateral side to the TBI, were successfully relieved with motor cortex stimulation (MCS). The analgesic effect of stimulation was found to be long lasting and was still present at the 12-month follow up. As shown in this patient, the occurrence of central pain syndrome should be considered by physicians caring for TBI patients, and a comprehensive, systematic study will be needed to determine the prevalence of central pain after a TBI.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
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