Intracerebral Space-occupying Lesions Research Articles

Attenuation of circulatory and airway responses to endotracheal extubation in craniotomies for intracerebral space occupying lesions: Dexmedetomidine versus lignocaine

Objectives:The objective of the study is to compare the effect of dexmedetomidine versus lignocaine in attenuation of circulatory and airway responses during endotracheal extubation in craniotomies for intracerebral space occupying lesions (ICSOL).Materials and Methods:A total of 50 patients of American Society of Anesthesiologists Grade I and II of either sex, aged 18-50 years undergoing craniotomies for non-vascular ICSOL under general anesthesia were divided into two groups according to drug received. Group D (n = 25) received dexmedetomidine (0.5 mcg/kg) whereas group L (n = 25) received lignocaine (1.5 mg/kg). Both the drugs were given 5 min before the extubation over a period of 60 s. Values for heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), were recorded just before (A0) and 1, 3, 5 (A1, A3, A5) min after the study drug administration, at extubation (E) and 1, 3, 5, 10, 15 min after extubation (E1, E3, E5, E10 and E15). Respiratory rate, oxygen saturation and airway responses like coughing, breath-holding, laryngospasm/bronchospasm were recorded only at extubation (E) and 1, 3, 5, 10, 15 min after extubation (E1, E3, E5, E10, E15). Quality of extubation was recorded with four point scale. After extubation all these patients were also observed for sedation by Ramsey sedation score.Results:Both groups showed a statistically significant increase (D < L) in HR, SBP and DBP during (E) and immediately after extubation (E1) (P < 0.05). Dexmedetomidine (72%) produced a higher degree of sedation (Grade 3) as compare with lignocaine (0%) and with no incidence of coughing or breath holding (P < 0.05).Conclusion:Single dose of dexmedetomidine (0.5 mcg/kg) given 5 min before extubation produced significant attenuation of circulatory and airway responses produced during extubation as compared to Lignocaine (1.5 mg/kg) in ICSOL.

Reversible posterior leukoencephalopathy syndrome

A 40-year-old woman presented with headache, lethargy,dysarthria, diplopia and altered mental status. Her pastmedical history was significant for cystic fibrosis for whichshe underwent bilateral lung transplantation 3 years priorto admission. Her medications included tacrolimus andprednisone. On physical examination, she was afebrile andnormotensive without neck stiffness; she was intubated andon mechanical ventilation. Her MRI brain with intravenousgadolinium showed symmetric hyperdense signals withinthe white matter involving parietal (Fig. 1a), occipital(Fig. 1b) and cerebellar regions (Fig. 1c), without intrace-rebral space-occupying lesions. Cerebrospinal fluid (CSF)studies revealed clear and colorless fluid with normalopening pressure, cell counts, glucose and protein. Evalu-ation for infections, including routine blood cultures, CSFGram’s stain and cultures, VDRL, cryptococcal antigen,cytomegalovirus (CMV) polymerase chain reaction (PCR)assay, Epstein–Barr virus (EBV) PCR, human herpes virus-6 (HHV-6) PCR and JC virus PCR, was, however, unre-vealing. Serum tacrolimus drug level was 5 ng/ml (normal5–20 ng/ml). The clinical diagnosis of tacrolimus-associ-ated reversible posterior leukoencephalopathy syndrome(RPLS) was entertained given the negative infectious dis-eases workup. Tacrolimus was cautiously tapered off overa week, and her neurological condition slowly improved.Repeat MRI brain imaging a week after complete discon-tinuation of the tacrolimus showed the resolution of thehyperintense lesions (Fig. 1d, e).RPLS, also known as posterior reversible encephalopa-thy syndrome (PRES), is a clinical syndrome of varyingetiologies, but with similar neuroimaging findings. Char-acteristic clinical manifestations include non-localizedheadache unresponsive to analgesics, altered mental status,visual disturbances and seizures [1, 2]. RPLS is frequentlyassociated with acute hypertension, preeclampsia oreclampsia, sepsis, renal failure, thrombotic thrombocyto-penic purpura, hypercalcemia, hypomagnesium, autoim-mune diseases, cytotoxic therapies andimmunosuppressants [2]. Because of widespread use ofcalcineurin inhibitors (cyclosporine and tacrolimus) inpatients with solid organ transplantation (SOT) to preventorgan rejection, neurotoxicity of these agents has beenincreasingly reported, although the incidence of RPLSamong patients with SOT is low (0.5 %) [3]. The under-lying pathophysiology of RPL is poorly defined. Hypoth-eses include cerebral ischemia from vasospasm, disorderedcerebral autoregulation and endothelial dysfunction [1, 2].RPLS associated with calcineurin is thought to result fromdirect toxic injury to vascular endothelium, leading toproduction of inflammatory cytokines and capillary leak-age, which triggers vasogenic cerebral edema [1, 3, 4].Hypertension and high serum tacrolimus level are com-monly associated with RPLS but there are reported RPLScases with normal blood pressure and normal serum ta-crolimus drug concentrations [5]. Brain MRI, particularlyfluid-attenuated inversion recovery (FLAIR) and diffusion-weighted imaging (DWI) sequences, is the imagingmodality of choice of diagnosing RPLS. Typical MRIfindings are symmetrical white matter changes primarily

Clinical analysis of 42 cases of chronic expanding intracerebral hematoma

To summarize our own experiences of managing chronic expanding intracerebral hematoma (CEICH) and discuss its diagnosis and treatment. The courses of CEICH, clinical and imaging features, intraoperative findings, pathological examinations and follow-up outcomes were reviewed retrospectively. The relevant literatures were reviewed simultaneously. The course of CEICHs ranged from 22 days to 10 years. Twenty-three cases (54.8%) were misdiagnosed as cystic gliomas, cystic gliomas, brain cysticercoses, brain abscesses and tumor strokes, etc. The misdiagnostic rate had decreased to 19.0% since June 1997. Thirty-eight patients underwent surgical operations and 4 had puncture drainage of hematoma. There was no operative death. Thirty-three cases achieved an excellent recovery and 9 cases had varying degrees of nervous dysfunctions. The follow-up period was 1-21 years. One patient had recurrence after 10 years. Among the cases of multiple CEICH, two lesions underwent no surgical treatment. One increased obviously after 7 years and another disappeared. The following five points may be used as the diagnostic criteria of CEICH: (1) intracerebral cystic space-occupying lesions on brain images; (2) circular or circle-like enhancement around lesions; (3) a mixed signal of concentric circular lamellar structures on MRI T1WI; (4) abnormal vascular lesions on CTA, MRA or DSA; (5) clinical signs and symptoms of slow progress of intracranial pressure. CEICHs with clinical symptoms of local mass effect shall be obliterated surgically. The abnormal tissues in cyst wall of hematoma should be resected. Small hematomas (< 2 cm) may be followed up.

Role of foetal MRI in the evaluation of ischaemic-haemorrhagic lesions of the foetal brain

The purpose of this study is to define the role of foetal magnetic resonance imaging (MRI) in evaluating cerebral ischaemic-haemorrhagic lesions and the extension of parenchymal injuries. From September 2006 to September 2010, 271 foetal MRI have been performed on cases referred to us for ultrasound suspect of brain abnormalities or cytomegalovirus infection and Toxoplasma serum conversion. Foetal MRI was performed with a 1.5-T magnet system without mother sedation. Foetal MRI detected ischaemic-haemorrhagic lesions in 14 of 271 foetuses, consisting of 5% incidence. MRI confirmed the diagnosis in three of 14 cases with ultrasonography (US) suspect of ischaemic-haemorrhagic lesions associated with ventriculomegaly. In one of 14 cases with US findings of cerebellar haemorrhage, MRI confirmed the diagnosis and provided additional information regarding the parenchymal ischaemic injury. In eight of 14 cases with US suspect of ventriculomegaly (3), corpus callosum agenesis (2), hypoplasia of cerebellar vermis (1), holoprosencephaly (1) and spina bifida (1), MRI detected ischaemic and haemorrhagic lesions unidentified at US examination. In two of 14 foetuses with US suspect of intracerebral space-occupying lesion, MRI modified the diagnosis to extra-axial haematoma associated with dural sinus malformation. Results were compared with post-mortem findings or afterbirth imaging follow-up. Foetal MRI is an additional imaging modality in the diagnosis of cerebral ischemic-haemorrhagic lesions, and it is useful in providing further information on the extension of the parenchymal injury and associated abnormalities, thus improving delivery management.

Chronische cholestatische Hepatopathie und Grand-mal-Anfall

A 48-year-old woman was hospitalised because of grand-mal seizures. 3 years previously a malignant melanoma had been resected from the skin of the back. She was also known to have chronic cholestasis of unknown cause. On physical examination there were postictal signs, but no neurological abnormalities and no jaundice. Biochemical tests demonstrated greatly increased alkaline phosphatase (576U/I). gamma-GT (1556U/I) and leucine aminopeptidase (258U/I). The transaminases were only slightly raised (GOT 113U/I, GPT 82U/I). Magnetic resonance imaging of the brain revealed a single intracerebral space-occupying lesion, compatible with a melanoma metastasis. Endoscopic retrograde cholangiopancreatography discovered a filiform, short stenosis in the choledochal duct, histologically an adenocarcinoma. The cerebral metastasis was removed stereotactically without complications. A Whipple-type gastroduodenopancreatectomy was performed 2 months later. Histology of an intraoperative liver biopsy revealed Caroli's syndrome (focal intrahepatic biliary dilatation) with congenital hepatic fibrosis. Cholestasis persisted after the operation and was treated with ursodeoxycholic acid. The patient has now been free of symptoms for 3 years. Caroli's syndrome should be included in the differential diagnosis of chronic cholestasis of unknown cause. The case also demonstrates the justification, under certain conditions, of aggressive treatment even when there are two different malignancies.

MR-Spektroskopie bei Hirntumoren

MRT allows the anatomical visualization of intracerebral space-occupying lesions, and when magnetic resonance spectroscopy (MRS) is used in routine clinical practice it can give more information and be helpful in the diagnosis of such lesions. In MRS with long echo times for nerve tissue there are five metabolites that are particularly significant: N-acetyl aspartate (NAA), creatine, choline, lactate, and lipids. NAA levels are lowered in the presence of intracerebral tumors. Creatine is lowered in situations of hypermetabolic metabolism and elevated in hypometabolic conditions, but remains constant in many pathologic states and can be used as a reliable reference value. With malignant tumors there are usually elevated choline concentrations, reflecting increased membrane synthesis and a higher cell turnover. The lactate level rises following a switch in metabolism from aerobic to anaerobic glycolysis, and this is frequently observed in the presence of malignant tumors. The occurrence of lipid peaks in a tumor spectrum suggests the presence of tissue necroses or metastases. There are typical constellations that are seen on MRS for individual tumors, which are discussed in detail in the present paper.

Pseudotumour Cerebri

Benign or idiopathic intracranial hypertension, also termed 'pseudotumour cerebri', is defined by the presence of raised intracranial pressure (ICP) in the absence of a focal intracerebral space-occupying lesion. The signs and symptoms of elevated intracranial pressure are also observed such as headaches, nausea and vomiting, elevated arterial pressure and, often, bradycardia. Somnolence and palsy of the abducens nel ve are occasionally observed, while papilloedema causing reduction of visual acuity and blindness is a particularly defining feature.

Gamma Knife Radiosurgery in AIDS-Related Primary Central Nervous System Lymphoma

The frequency of AIDS-associated primary central nervous system (PCNS) lymphoma is rapidly increasing in adults and children. In AIDS-related PCNS lymphoma, different authors have reported an overall poorer response rate to conventional radiation compared with immunocompetent patients. This poorer response consists of a significantly positive, although transient effect on survival following radiotherapy (XRT), with a poor toleration for prolonged whole-brain RT (WBR) and with radiation-induced changes within the normal CNS tissue on autopsy examinations after a course of XRT. These observations led us to consider highly focused single-session radiosurgical treatments as a potentially useful therapeutic modality for AIDS-associated PCNS lymphomas. A multi-institutional diagnostic and therapeutic protocol for the evaluation and treatment of AIDS patients with high-risk intracerebral space-occupying lesions has been developed at the University Hospital of Verona. Therapy is based on tumor biopsy. Tumors < or = 3.5 cm in diameter are subjected to Gamma Knife radiosurgery, whereas tumors < or = 4.5 cm are treated with stereotactic brachytherapy. At the Department of Neurosurgery, Verona, Italy, Gamma Knife treatment was performed in 2 cases of deep-seated histologically verified malignant non-Hodgkin's lymphoma. A short-term cliniconeuroradiological follow-up (2 months later) showed neurologic improvement and virtually complete disappearance of the tumor in both patients. The excellent local control and the well-tolerated single-session treatment and absence of brain toxicity signs on CT scan indicate a putative role for Gamma Knife radiosurgery in the treatment of these patients.

Neurosurgery with craniotomy and CT stereotactic guidance in the treatment of intracerebral space-occupying lesions

When intracerebral space-occupying lesions are small or located deeply within the brain parenchyma, it is sometimes difficult to localize them at surgery or to design the most direct and least hazardous surgical approach. Therefore, we have developed a method that combines conventional neurosurgical techniques with craniotomy using stereotactic guidance. We have used the Brown-Roberts-Wells (BRW) stereotactic system, which allows for computed tomography (CT) or magnetic resonance imaging (MRI) guidance and does not interfere with the absolute sterility mandatory each time a flap is created. Eleven patients were operated on using this method. The deep tumors were approached through a linear incision of the cerebral cortex. Then a needle, fixed in the right position on the arc system of the BRW, was inserted toward the surface of the lesion; the exposure was finally widened by inflation of a rubber balloon set on the stereotactic needle. This technique allows the two lips of the cortical incision to be glued at the end of the operation. Gluing with a fibrin glue avoids the postoperative subdural collections that often develop when the ventricle has been opened. Except for one case, the postoperative course was uncomplicated in these patients. No permanent postoperative neurological worsening was observed even after the removal of an intrathalamic tumor.

Experimental intracerebral haematoma: The role of blood constituents in early ischaemia

In patients with intracerebral haematoma, ischaemic damage and final outcome are often more serious than the size of the lesion would suggest. The aetiology of the ischaemia in relation to space-occupying effects or specific factors present in blood is unclear. In a rat model of an intracerebral space-occupying lesion, the pathophysiological effects of a haematoma were compared with those of an equal volume of inert fluid (mock cerebrospinal fluid [CSF] or silicone oil). Cerebral blood flow was measured at 1 min by 14C iodoantipyrine autoradiography, and ischaemic cell damage was assessed by light microscopy at 4 h. In all animals, cerebral blood flow was reduced immediately adjacent to the lesion. In the group with a haematoma, blood flow was reduced (p less than 0.001) over a greater radius and also in the ipsilateral frontal and parietal cortex. Ischaemic damage was seen in animals lesioned with blood or oil of blood viscosity, but not in animals with CSF lesions. These data suggest that both tissue pressure and vasoactive substances are components of the immediate reduction in blood flow following intracranial haemorrhage. Tissue pressure may be the more important factor in later ischaemic neuronal damage.

Experimental intracerebral hemorrhage: progression of hemodynamic changes after production of a spontaneous mass lesion.

The aim of the study was to determine whether the extent of ischemia produced by an experimental space-occupying lesion changed between 5 minutes and 4 hours after the production of a lesion. In two groups of rats, a 50-microliter balloon was inflated in the right caudate nucleus. Cerebral blood flow (CBF) was determined by 14C-iodoantipyrine quantitative autoradiography, in Group 1 (n = 6) 5 minutes after inflation and in Group 2 (n = 6) 4 hours later. After 5 minutes of inflation, the mean blood flow in the caudate nucleus was reduced to 65% of the contralateral value and 11.5% of the ipsilateral caudate nucleus had a blood flow of below 25 ml/100 g/minute. After 4 hours of inflation, there was a greater fall in the mean CBF of the ipsilateral caudate nucleus to 30% of the contralateral value, and 38.9% of the ipsilateral caudate nucleus had a CBF of less than 25 ml/100 g/minute. The differences between the two groups were significant (mean CBF, P less than 0.01; CBF less than 25 ml/100 g/minute, P less than 0.02). The results show that the initial ischemic lesion produced by a spontaneous intracerebral space-occupying lesion does not remain static, but progresses with time and is significantly greater after 4 hours than after 5 minutes. Interventions that reduce the progression of ischemia may be beneficial in reducing the ultimate amount of ischemic brain damage.

Dural sinus and cerebral venous thrombosis.

Eighty patients with 'primary' dural sinus and cerebral venous thrombosis were seen over a period of 16 years. There was an equal distribution amongst the sexes and the largest number of patients presented in the third decade. The commonest predisposing factors were puerperium, pregnancy, synthetic steroid contraceptives and anaemia. Seventy patients presented in an acute fashion with headache, focal or generalized seizures and focal neurological deficits. Ten patients presented in a subacute to chronic manner, with features to suggest an intracerebral space-occupying lesion. The investigation of choice was angiography. Thirty-five patients were treated conservatively with anticonvulsants, low molecular weight dextran and anti-oedema measures. Anti-coagulants were not used for fear of haemorrhage in the associated red infarcts. Antibiotics were not needed as infection played no part in the pathogenesis. Thirty-four patients needed an operation which took the form of a decompressive craniotomy and dural closure with the aid of a pericranial graft. The conservatively treated group appeared to fare better only because it included patients with a milder ictus. Forty patients improved, three remained unchanged and 37 expired. Autopsy in the 35 of the 37 patients showed cortical vein and sinus thrombosis and oedema with a haemorrhagic infarct. Long term follow-up showed good recovery of neurological function, but epilepsy was a troublesome sequel and needs regular anti-epileptic drug treatment.

Adult Onset Epilepsy and History of Childhood Febrile Convulsions: A Retrospective Study

Objective: To assess the association between adult -onset epilepsy and history of childhood febrile convulsions (CFC) and determine the types of epilepsy which develop after CFC Design: A retrospective study. Study period: January 2008 to December 2008. Place of study: Epilepsy Clinic of the Department of Neurology of Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka. Materials &amp; Methods: 106 consecutive adult (age&gt;13 years) patients with adult onset epilepsy receiving treatment from Epilepsy Clinic of the Department of Neurology of BSMMU, Dhaka were the sample of this study. Records of these patients were reviewed &amp; the patients &amp; their family members were interviewed to assess the medical history. The data obtained from the records and the interviews formed the basis of this study. Chi-Square test was applied to analysis the data. Results: Results of interview and records of 92 patients were analyzed. Of the 106 patients 14 patients were excluded from this study for the reasons of missing reliable data of the CFC episodes (9), secondary epilepsy due to intracerebral space occupying lesions (ICSOL) (1), history of head injury (1) &amp; meningoencephalitis (3). Thirty one (33.7%) of the remaining ninety two patients had history of CFC in the childhood (71% male, 29% female). Partial epilepsies were significantly associated with history of CFC [Odds Ratio : 3.29; (95% CI 1.30-8.06), (c2=5.49, df=1, p&lt;0.012)] when compared to other epilepsies and epilepsy syndromes. An initial unprovoked simple partial seizure was also significantly associated with a positive history of CFC [Odds Ratio : 8.05; (95% CI 2.88-22.45), (c2=15.86, df=1, p&lt;0.001)]. Conclusion: Partial epilepsies seem to be associated with a history of CFC in childhood. The mechanism &amp; pathophysiology of association between CFC and epilepsy in affected probands requires further investigations. Identification of the basic defect in relation to CFC &amp; epilepsy may have important implication for the prevention of adult- onset epilepsy in patients with history of CFC. But the risk of epilepsy after febrile convulsions is much less than reported in many hospital studies &amp; if febrile convulsion causes brain damage that leads to epilepsy later, this is a rare occurrence. Key words: Generalized epilepsy; partial epilepsy; febrile convulsion; afebrile seizures; genetic. DOI: 10.3329/jdmc.v18i1.6307 J Dhaka Med Coll. 2009; 18(1) : 54-57

The superficial sylvian vein in normal and pathologic cerebral angiography.

The angiographic patterns of the normal course and variations of the superficial sylvian vein (s.s.v.) are reviewed.The pathologic alterations of these patterns are considered for extracerebral and intracerebral space-occupying lesions and some exceptions to commonly accepted diagnostic criteria are made and illustrated.