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D Tampieri

Publications and source records attributed to D Tampieri.

At least 19 recordsLinked to original sources
PubMed2005

Etomidate speech and memory test (eSAM): a new drug and improved intracarotid procedure.

BACKGROUND: The intracarotid amobarbital procedure (IAP) is an important part of comprehensive investigation of patients who are candidates for surgical treatment of epilepsy. Owing to repeated and lengthy shortages of amobarbital, causing delays in elective surgery, attempts have been made to find a suitable alternative anesthetic. The authors report their experience using etomidate, a widely used agent for the induction of anesthesia. METHODS: Sixteen consecutive patients requiring IAP to evaluate memory or to lateralize speech underwent the procedure using etomidate. Prior to the procedure a catheter was placed in the internal carotid artery and an angiogram was performed. EEG was recorded and read online by an electroencephalographer. An anesthetist injected the drug, administered by bolus followed by an infusion, which was maintained until each speech measure had been sampled and new memory items had been introduced. The infusion was then stopped and testing continued as in a standard IAP. RESULTS: In all cases (30 hemispheres) contralateral hemiplegia followed injection. EEG slow waves were observed in every injected hemisphere, with some contralateral slowing anteriorly in 18. Global aphasia with preserved attention and cooperation followed dominant-hemisphere injections. These phenomena remained during infusion, and upon its termination returned gradually to baseline over a period of about 4 minutes. CONCLUSIONS: Etomidate is a viable alternative to amobarbital, and its administration by bolus followed by infusion offers an improvement over the traditional intracarotid amobarbital procedure. Cognitive tests can be performed during an assured hemianesthesia of the injected hemisphere.

Adolescent↗
PubMed2001

The role of MRI and nerve root biopsy in the diagnosis of neurosarcoidosis.

OBJECTIVES: Neurological involvement occurs in 5-15% of patients with sarcoidosis and isolated "neurosarcoidosis" occurs in less than 1% of all cases. Classical clinical presentations have been described, such as bilateral facial palsy, but often the disease presents insidiously with varied signs and symptoms. We present a patient who required biopsy of a lumbar nerve root for diagnosis of chronic, progressive neurosarcoidosis and review the literature with an emphasis on diagnosis. METHODS: We have reviewed a patient who presented with signs and symptoms related to infiltration of her meninges and nerve roots by sarcoidosis. All pertinent history and physical information was taken from interviews with the patient and review of her chart. Laboratory, radiographic, and pathological investigations are presented. RESULTS AND CONCLUSIONS: A high index of suspicion is required for the diagnosis of neurosarcoidosis. Gadolinium-enhanced MRI is useful but the findings are often nonspecific, and there should be a low threshold for biopsy whenever the diagnosis is considered.

Biopsy, Needle↗
PubMed2001

Rathke's cleft cyst presenting as sphenoid sinusitis.

Rathke's cleft cysts are developmental abnormalities of the craniopharyngeal duct composed of retained stratified ciliated cuboidal cells of the respiratory type. Incidentally found in the pars intermedia in 13% to 33% of routine autopsies, they are discovered in growing numbers on CT and MRI scans. From 1991 to 1999, 9 cases of Rathke's cleft cysts were encountered by the senior authors, 4 of which were treated surgically (3 by using a transsphenoidal approach and one by using a transcranial subfrontal approach). Of the 3 patients treated with a transsphenoidal approach, 2 presented with symptoms mimicking sphenoid sinusitis and were initially referred for otolaryngologic evaluation. The clinical, pathologic, and radiologic features, as well as management and follow-up of those 2 patients, are reviewed. There has been only one previous case report of Rathke's cleft cysts presenting as sinusitis. Nevertheless, the otolaryngologist should be aware of this condition because it may present with other significant symptomatic extracranial extensions.

Adult↗
PubMed2001

Mycotic aneurysm of the carotid bifurcation in the neck: case report and review of the literature.

OBJECTIVE AND IMPORTANCE: Mycotic aneurysms of the extracranial carotid artery are rare and difficult to diagnose. A search of the world literature published since 1966 reveals at least six cases of mycotic carotid aneurysms due to a Salmonella septicemia. We present an exceptional case of mycotic pseudoaneurysm of the bifurcation of the carotid artery due to Salmonella septicemia and discuss the pathogenesis as well as various aspects of the diagnosis and surgical management. CLINICAL PRESENTATION: A 68-year-old man presented in Poland with Salmonella sepsis; 1 month later, he was admitted to the emergency department of the Sir Mortimer B. Davis-Jewish General Hospital in Montreal with a bulky and pulsatile right cervical mass. An angiogram and a computed tomographic scan revealed a voluminous and partially thrombosed aneurysm the size of a tangerine originating from the posterior aspect of the carotid junction. INTERVENTION: Balloon trapping was attempted at the Montreal Neurological Hospital. Subsequently, the patient developed a significant neurological deficit, which was quickly reversed by the administration of hypertensive, hypervolemic, and hemodilution therapy. Thereafter, the pseudoaneurysm was resected surgically, and the internal and external carotid arteries were sacrificed. Pathological examination of the excised specimen of the carotid junction revealed a pseudoaneurysm. Bacterial culture of the lesion showed growth of Salmonella. CONCLUSION: The postoperative course was satisfactory except for laryngeal paralysis due to involvement of the vagus nerve. Four months later, a computed tomographic scan showed only small lacunae in both centra semiovale.

Aged↗
PubMed2000

T2 relaxometry can lateralize mesial temporal lobe epilepsy in patients with normal MRI.

In unselected patients with intractable temporal lobe epilepsy (TLE), approximately 15% do not have detectable hippocampal atrophy on MRI. The purpose of this study was to evaluate whether T2 relaxometry can identify hippocampal pathology and lateralize the epileptic focus in patients with intractable TLE, who do not demonstrate hippocampal atrophy on volumetric MRI (MRIV). We selected 14 patients with unilateral TLE who had unilateral atrophy and 11 patients with unilateral TLE who had no evidence of atrophy on MRIV. Images were acquired on a 1.5 T MR scan using a dual echo sequence with 23 contiguous oblique coronal slices in all patients and in 14 healthy subjects. Fitting a single exponential decay equation to the imaging data generated T2 maps. Averages of six slices containing the head, body, and tail of the hippocampus were used to calculate hippocampal T2 relaxation times (HT2). The epileptic focus was defined by history, video-EEG, and surgical response. All TLE patients with hippocampal atrophy and 9/11 (82%) patients with normal MRI had abnormally high HT2 ipsilateral to the epileptic focus. Bilateral abnormal HT2 were found in 6/14 (43%) of patients with unilateral hippocampal atrophy and 2/11 (18%) of patients with normal MRI. However, this increase was always greater ipsilateral to the epileptic focus. Qualitative hippocampal pathology showed gliosis and neuronal loss in 10/14 operated patients with hippocampal atrophy on MRIV and in 5/7 operated patients with normal MRI. In conclusion, hippocampal T2 mapping provides evidence of hippocampal damage in the majority of patients with intractable TLE who have no evidence of atrophy on MRI and can correctly lateralize the epileptic focus in most patients.

Adult↗
PubMed1999

Diagnosis of subtle focal dysplastic lesions: curvilinear reformatting from three-dimensional magnetic resonance imaging.

Focal cortical dysplasia is a frequent cause of medically intractable partial epilepsy. These lesions are being increasingly identified by high quality images provided by magnetic resonance imaging (MRI), resulting in improved seizure control of surgically treated patients. Small dysplastic lesions are often missed by conventional MRI methods. The identification of subtle structural abnormalities by rectilinear slices is often limited by the complex convolutional pattern of the brain. We developed a method of curvilinear reformatting of three-dimensional MRI data that improves the anatomical display of the gyral structure of the hemispheric convexities. It also reduces the asymmetric sampling of gray-white matter that may lead to false-positive results. We present 5 patients in whom conventional two-dimensional and three-dimensional MRI with multiplanar reformatting was initially considered normal. Subsequent studies using curvilinear reformatting identified lesions in all. Four patients underwent surgery with histological diagnosis of focal cortical dysplasia. Three patients are seizure-free and 1 had significant improvement in seizure control. These results indicate that an increase in the detection of subtle focal dysplastic lesions may be accomplished when one improves the anatomical display of the brain gyral structure by performing curvilinear reformatting.

Adolescent↗
PubMed1999

The various MRI patterns of pituitary apoplexy.

The aim of this study was to describe the various MRI features, in correlation to surgical and pathological findings, in patients who presented with pituitary apoplexy (PA). Eleven patients presenting with PA, were evaluated with various MR protocols including spin-echo (SE) T1-weighted sequences in 9 of 11 patients, post gadolinium SE T1-weighted sequences in only 8 of 11 patients, and with T2-weighted SE sequences in 2 of 11 patients. All patients had transsphenoidal pituitary surgery after MR studies. The severity of presenting symptoms ranged from headaches to coma. Ten patients had pituitary macroadenoma; one had a non-hemorrhagic metastatic lesion into a non-adenomatous pituitary gland. Of the 11 patients, one was studied at the acute stage of PA (1 day after onset), 9 at the subacute period (3-15 days after onset), and one at the late stage (5 months after onset). Images compatible with intratumoral hemorrhage were found in all macroadenomas, whereas the metastatic pituitary lesion did not show evidence of bleeding. All gadolinium-enhanced studies showed partial tumoral enhancement. The SE T2-weighted studies demonstrated areas of low and high signal intensities in keeping with the presence of blood degradation contents. Pituitary apoplexy present with different MR features, including hemorrhagic and non-hemorrhagic characteristics on T1-weighted images. Gadolinium-enhanced images do not provide complementary diagnostic information when the presence of blood is assessed on plain images.

Adult↗
PubMed1999

Relationship between O6-methylguanine-DNA methyltransferase levels and clinical response induced by chloroethylnitrosourea therapy in glioma patients.

BACKGROUND: Adjuvant nitrosourea chemotherapy fails to prolong survival significantly as many tumors demonstrate resistance to these drugs. It has been documented in cell lines that O6-methylguanine DNA methyltransferase (MGMT) plays an important role in chloroethylnitrosourea (CENU) drug resistance. METHODS: We evaluated MGMT expression in 22 glioma specimens by using an immunofluorescence assay and compared the results with clinical responses of the patients to CENU-based chemotherapy. RESULTS: Eight tumor samples had no detectable MGMT, whereas other samples had from 9,989 to 982,401 molecules/nucleus. In one group (12 patients), the tumor decreased in size or was stable (effective group), whereas in the other group (10 patients), the tumor demonstrated continuous growth during chemotherapy (progressive group). The Mer- patients (MGMT < 60,000 molecules/nucleus) appeared to have more chance of stable disease or response to CENU therapy than the Mer+ patients (MGMT > 60,000 molecules/nucleus) (X2 = 4.791, p = 0.0286). In patients with glioblastomas multiforme (GBMs), the median time to progression (TTP) of Mer+ patient was shorter than that of Mer- patient (t = 2.04, p = 0.049). As a corollary, the MGMT levels were significantly higher in GBM tumors from the progressive group than those from the effective group (t = 2.26, p = 0.029). However, there was no significant correlation between MGMT levels and either the survival time (r = 0.04, p = 0.8595) or TTP (r = 0.107, p = 0.6444). CONCLUSION: This study suggests that being MGMT positive is indicative of a more aggressive disease that progresses more rapidly with CENU therapy. However, MGMT negative tumors are not always sensitive to CENU agents, suggesting that other factors are also important.

Adult↗
PubMed1999

Juvenile nasopharyngeal angiofibroma.

This is a retrospective study of 17 patients with juvenile nasopharyngeal angiofibroma treated from 1983 to 1996. Patients with Stage I or II disease according to the Fisch classification system were treated surgically by a transpalatal approach. One patient underwent a Le Fort I osteotomy and down-fracture approach for access. Three patients underwent combined transpalatal and lateral rhinotomy for access, whereas one underwent a transcervical double mandibular osteotomy to facilitate the exposure. A patient with Stage IV disease underwent a combined subcranial frontonasal osteotomy plus a Le Fort I osteotomy for access to a massive angiofibroma. Initial surgical management prevented recurrence in 79% of patients. Two patients with intracranial extension were treated with primary irradiation therapy; their tumours became asymptomatic. Preoperative angiography and embolization were used to treat all surgical candidates. The use of newer craniofacial or subcranial techniques and infratemporal fossa approaches with osteotomies can provide access to large angiofibromas even when there is skull base or intracranial involvement. Surgical exposure may also be enhanced by the use of the Le Fort I osteotomy and down-fracture approaches.

Adolescent↗
PubMed1998

Clinical response of O(6)-methylguanine-DNA methyltransferase levels to 1,3-(2-chloroethyl)-1-nitrosourea chemotherapy in glioma patients.

Adjuvant nitrosourea chemotherapy fails to prolong patient survival significantly as many tumors demonstrate resistance to these drugs. It has been documented in cell lines that O(6)-methylguanine-DNA methyltransferase (MGMT) plays an important role in chloroethylnitrosourea (CENU) drug resistance. The authors evaluated MGMT expression in 22 glioma specimens by using an immunofluorescence assay and compared the results with clinical response of the patients to CENU-based chemotherapy. The patients were treated with CENU after evidence of progressive disease following surgery and radiotherapy. Eight tumor samples had no detectable MGMT, whereas other samples had from 9989 to 982,401 molecules/nucleus. In one group (12 patients), the tumor decreased in size or was stable (effective group), whereas in the other group (10 patients), the tumor demonstrated continuous growth during chemotherapy (progressive group). The median time to progression (TTP) was 6.7 months with a median survival of 13 months. The Mer(-) patients (MGMT < 60,000 molecules/nucleus) appeared to have more chance of stable disease or response to CENU therapy than the Mer(+) patients (MGMT > 60,000 molecules/nucleus) (chi-square = 4.791, p = 0.0286). In patients with glioblastomas multiforme (GBMs), the TTP of Mer(+) patients was shorter than that of Mer(-) patients (t = 2.04, p = 0.049). As a corollary, the MGMT levels were significantly higher in GBM tumors from the progressive group than those from the effective group (t = -2.26, p = 0.029). The TTP and survival time in the effective GBM group were also longer than those in the progressive GBM group. However, there was no significant correlation between MGMT levels and either the survival time (r = 0.04, p = 0.8595) or TTP (r = 0.107, p = 0.6444). Results from this study suggested that MGMT positivity is indicative of more aggressive disease that progresses more rapidly when exposed to CENU therapy. However, MGMT-negative tumors are not always sensitive to CENU agents, suggesting that other factors may also be important.

Journal Article↗
PubMed1998

Cortical dysplasia: an immunocytochemical study of three patients.

Human cortical dysplastic lesions are frequently associated with severe partial epilepsies. We report an immunocytochemical investigation on cortical tissue from three surgically treated patients, 20, 38, and 14 years old, with intractable epilepsy due to cortical dysplasia. The studies were performed using antibodies recognizing cytoskeletal proteins, calcium-binding proteins, and some subunits of glutamate receptors. The specimens from the three patients displayed common features: (1) focal cytoarchitectural abnormalities with an increased number of giant pyramidal neurons through all cortical layers except layer I; (2) large, round-shaped balloon cells mainly concentrated in the deepest part of the cortex and in the white matter; (3) a decrease of calcium binding protein immunopositive gamma-aminobutyric acid (GABA)ergic neurons; and (4) abnormal baskets of parvalbumin-positive terminals around the excitatory (pyramidal and large, round-shaped) neurons. These data provide evidence that the epileptogenicity in these types of cortical dysplasia is due to an increase in excitatory neurons coupled with a decrease in GABAergic interneurons.

Adolescent↗
PubMed1997

Assessment of the functional effect of the intracarotid sodium amobarbital procedure using co-registered MRI/HMPAO-SPECT and SEEG.

We studied the functional effect of injection of sodium amobarbital (SA) in 10 patients with intractable epilepsy. During the intracarotid amobarbital procedure, we measured delta activity in EEG recording from implanted electrodes and regional cerebral blood flow (rCBF) using HMPAO-SPECT co-registered with MRI. SA injection resulted in an increase in delta activity and a decrease in rCBF in all areas examined. Direct functional changes were observed in structures perfused by the carotid artery injected. In addition, we observed indirect effects, probably owing to deafferentation of neuronal pathways connecting these structures to ipsilateral and contralateral regions, including middle and posterior hippocampus.

Amobarbital↗
PubMed1996

Low-grade pure and mixed cerebral astrocytomas treated in the CT scan era.

From 1974 to 1992, 63 patients diagnosed with low-grade pure or mixed oligo-astrocytoma were seen and treated at our institution. All patients underwent CT scan pre-operatively. There were 20 female and 43 males ranging in age from 12 to 73 years (median age of 33 years). 15 patients had a stereotactic biopsy as the only surgical procedure. 34 had a partial tumor resection and 14 a gross total tumor resection. 43 patients were treated with post-operative radiotherapy whereas 20 patients underwent surgery only as part of the initial management. 50 to 60 Gy (median 59.4 Gy) were given with daily fractions of 1.8 to 2 GY. Tumor volume ranged from 3.4 to 441 cm3. Median tumor volume was larger for radiotherapy treated patients. Median follow-up was 54 months (range of 4 to 240 months). The overall 10 and 15 actuarial survival rates were 37% and 25% respectively. The 5 years survival rate for patients treated at initial diagnosis with surgery alone was 66% and it was 67.3% for patients treated with radiation therapy (P = NS). Prognostic factors having independent significant impact on survival were: extent of surgery, age gender and tumor volume. As well, survival for patients with low-grade astrocytoma in the CT scan era appears to be improved compared to historical controls in the literature.

Adolescent↗
PubMed1996

The negative angiogram in subarachnoid haemorrhage.

Our purpose was to review the incidence of negative cerebral panangiography in acute nontraumatic subarachnoid haemorrhage (SAH); to document the amount and distribution of subarachnoid blood on CT and determine its relationship to findings on repeat angiography; and to study the outcome of these patients from the time of presentation to hospital discharge. From 1983 to 1992, 295 patients underwent cerebral angiography for acute SAH at our institution. The CT, angiographic and MRI findings and clinical course of patients with initially negative angiograms were reviewed retrospectively. The overall incidence of negative cerebral panangiography was 31% (92/295). An aneurysm was disclosed on a second angiogram in 4 cases, and on a third angiogram in 1, giving a total false negative rate of 5%. In 55% of cases, only a small amount of SAH was present on CT. The distribution of the subarachnoid blood was nonspecific and resembled the pattern seen in aneurysmal SAH. Ninety-four percent of the patients presented in Hunt-Hess grades I and II. The complications of conservative treatment were few: a rebleed rate of 4%, delayed cerebral ischemia in 4%, cerebral infarcts in 8% and hydrocephalus requiring shunting in 3%. On discharge, 93% of patients had recovered completely and the others were left with moderate disability. There were two deaths related to massive rebleeding. Patients with perimesencephalic SAH (35%) fared particularly well; none developed complications during their hospital stay and repeat angiograms never revealed an underlying aneurysm. In such cases, further angiographic investigations do not seem warranted.

Angiography, Digital Subtraction↗
PubMed1996

Neuronal migration disorders and epilepsy: a morphological analysis of three surgically treated patients.

Despite the increasing number of patients affected by neuronal migration disorders (NMDs) recently diagnosed in vivo by means of magnetic resonance imaging (MRI), few detailed data on the correlation between the neuroradiological and the anatomical features in the single NMD case are available. The present paper reports a combined cytoarchitectural and immunocytochemical analysis, by means of antisera recognizing specific neuronal and glial markers, of three MRI diagnosed NMD patients surgically treated for the relief of intractable seizures. The first case was a giant subcortical nodular heterotopia of morphologically normal neurons lacking any type of cortical lamination. The second case was a layered polymicrogyria with an abnormal amount of ectopic neurons in the underlying white matter. The third case was a focal cortical dysplasia characterized by a dramatic disruption of the normal cortical layering associated with marked cytological abnormalities. The present data demonstrate that the macroscopical and microscopical brain abnormalities can be markedly different in different NMD subtypes, and suggest that different anatomical substrates can underlie the intrinsic hyperexcitability of these brain malformations. The relevance of further prospective clinico-morphological studies for a better understanding of the mechanisms determining the development of these brain malformations is underlined.

Brain↗
PubMed1996

X-linked malformations of neuronal migration.

Malformations of neuronal migration such as lissencephaly (agyria-pachygyria spectrum) are well-known causes of mental retardation and epilepsy that are often genetic. For example, isolated lissencephaly sequence and Miller-Dieker syndrome are caused by deletions involving a lissencephaly gene in chromosome 17p13.3, while many other malformation syndromes have autosomal recessive inheritance. In this paper, we review evidence supporting the existence of two distinct X-linked malformations of neuronal migration. X-linked lissencephaly and subcortical band heterotopia (XLIS) presents with sporadic or familial mental retardation and epilepsy. The brain malformation varies from classical lissencephaly, which is observed in males, to subcortical band heterotopia, which is observed primarily in females. The XLIS gene is located in chromosome Xq22.3 based on the breakpoint of an X-autosomal translocation. Bilateral periventricular nodular heterotopia (BPNH) usually presents with sporadic or familial epilepsy with normal intelligence, primarily in females, although we have evaluated two boys with BPNH and severe mental retardation. The gene for BPNH has been mapped to chromosome Xq28 based on linkage studies in multiplex families and observation of a subtle structural abnormality in one of the boys with BPNH and severe mental retardation.

Adult↗