Published on February 27, 2014
SPACE OCCUPYING LESIONS OF THE BRAIN 16 DECEMBER 2013
CONTENT DEFINITION OF SOL TYPES OF SOL IN THE BRAIN SIGNS AND SYMPTOMS NEUROIMAGING AND OTHER INVESTIGATIONS TREATMENT PROGNOSIS
DEFINITION OF SOL Substantial physical lesions, e.g. neoplasm, hemorrhage, granuloma, which occupy space; the effect is more significant if the lesion is within a space confined by bone, e.g. thorax, cranium, bone marrow cavity. SOL OF THE BRAIN : Within the cranium or skull.
TYPES OF SOL IN THE BRAIN Neoplasm Infection Meningioma, glioma, pituitary tumour E.g. abscess, tuberculoma Vascular lesions AVM, cavernoma, giant aneurysm Hemorrhage
SIGNS AND SYMPTOMS Neurological phenomena is caused by irritation or destruction of brain tissue, e.g. Focal seizures (Jacksonian epilepsy) Paralysis. Headache Do not respond to simple medicines refers to the possibility of ICSOL. The headache is felt in the midline over the head of at times it is referred over the site of lesion, e.g meningioma. It will be continuous and progressive, paroxysmal (as in migraine), or aggravated by coughing, stooping forward and changing postures. Patients with headaches that wake them at night or are worse in the morning, or who have focal neurologic deficits, require urgent neuroimaging. However, many patients with brain tumours present with headaches that are indistinguishable from tension headaches.
SIGNS AND SYMPTOMS Vomiting and visual loss: In many cases, protracted vomiting is a common symptom. Projectile vomiting is mistaken for gastrointestinal or psychiatric disturbances. Failure of vision because of late papilloedema phenomenon. Impairment of conscious level due to raised intracranial pressure. Headaches, nausea, vomiting, and changes in mental status, cognition, and progressive altered levels of consciousness alongside other indicative signs such as papilloedema usually reflect raised intracranial pressure from mass effect or hydrocephalus. Late onset of seizures: Any type of seizure if occurs for the first time after the age of 15 years will suggest the possibility of ICSOL.
SIGNS AND SYMPTOMS Both nonspecific and focal neurologic complaints and symptoms can alert the primary care physician or neurologist to the possibility of an underlying mass lesion and indicate the need for further work - up. Key aspects of the history that help differentiate neoplastic lesions from other diagnoses include Timing of symptom onset, Tempo of progression, Severity of symptoms. Systemic symptoms and the presence of other diseases or hereditary syndromes are additional valuable pieces of information that can help narrow the diagnosis by their association with specific CNS tumours.
SIGNS AND SYMPTOMS Other symptoms and signs, such as global mental status changes, are quite common and include apathy, change in personality, irritability, psychomotor retardation, lethargy, and forgetfulness. Such nonspecific impairments in mental function have been linked to lesions in the frontal and temporal lobes, corpus callosum, thalamocortical fibers, and reticular formation, among others. Still other non-localizable presentations are the result of multifocal tumours, often seen in metastatic disease, presenting with a mixture of focal signs and symptoms that can be confused for generalized clinical manifestations.
SIGNS AND SYMPTOMS Brain tumour Symptoms produced by brain tumors may be either nonspecific or focal, and in general tend to be subacute in onset. The presentation varies widely and neither a normal neurologic exam nor presentation with acute onset of symptoms rules out a brain tumour. At the outset many brain tumours produce minimal or no symptoms. Brain tumors can also present with acute onset stroke - like symptoms.
SIGNS AND SYMPTOMS Brain tumour This type of acute presentation is usually the result of a focal seizure or hemorrhage into the tumour bed. The rate of progression of symptoms is also quite variable but tends to be gradual over weeks to months, helping to differentiate neoplasms from other more static disorders such as degenerative disease or more rapidly progressing infectious conditions. By paralleling the growth and spread of CNS neoplasms, the rate of symptomatic progression can serve as a rough clinical estimate to tumour grade.
SIGNS AND SYMPTOMS Brain tumour Typically, benign tumours such as meningiomas, or low grade neoplasms such as oligodendrogliomas, will have a slower progression of symptoms than more malignant tumours such as glioblastomas. A careful review of systems, for instance, should identify symptoms such as weight loss, lethargy, and night sweats that are nonspecific but can be associated with many types of cancers. When combined with neurologic symptoms, these symptoms should raise suspicion of primary or metastatic CNS neoplasms, though should not rule out subacute infectious, inflammatory, or autoimmune CNS processes.
SIGNS AND SYMPTOMS Brain tumour Likewise, a detailed review of past medical history may identify genetic syndromes or other conditions with a higher than normal incidence of CNS neoplasms. Neurofibromatosis type 1 is associated with gliomas and cutaneous manifestations, Neurofibromatosis type 2 is associated with vestibular schwannomas and meningiomas, Von Hippel – Lindau syndrome is associated with hemangioblastomas.
SIGNS AND SYMPTOMS Intracranial Infection The onset of acute bacterial meningitis is rapid: hours to a day or so. Classic clinical findings include signs of an acute cerebral disorder, with lethargy, seizures, and agitation as well as specific signs of meningeal involvement manifested by severe neck stiffness, called meningismus Fever that may not be immediately present. The patient rapidly becomes confused, sleepy, obtunded, and often comatose
SIGNS AND SYMPTOMS Intracranial Infection For identifying the presence of inflamed meningeal coverings involving the lumbosacral nerve roots: The Kernig sign is elicited by flexing the patient’s hip to a 90-degree angle and then attempting to passively straighten the leg at the knee; pain and tightness in the hamstring muscles prevent completion of this maneuver. This sign should be present bilaterally to support a diagnosis of meningitis. The Brudzinski sign is positive if the patient’s hips and knees flex automatically when the examiner flexes the patient’s neck while the patient is supine.
SIGNS AND SYMPTOMS Brain abscess The cardinal symptom of brain abscess is persistent and progressive headache, usually followed by focal neurologic manifestations. Only two thirds of patients have fever. Papilloedema and other signs of increased intracranial pressure may occasionally develop; however, the availability of imaging studies makes it more likely that the abscess will be identified prior to its obtaining significant enough mass to create increased intracranial pressure.
SIGNS AND SYMPTOMS Subdural abscess It is typically characterized by a purulent collection within the potential space between the dura mater and arachnoid membrane Localized swelling, erythema, headache, or tenderness of the site overlying the primary infection may occur. As the illness progresses, the headache becomes generalized and severe, with a high fever, vomiting, and nuchal rigidity developing. Seizures, hemiparesis, visual field defects, and papilledema sometimes occur.
SIGNS AND SYMPTOMS Intracranial Hemorrhage Intraparenchymal hemorrhages vary in presentation depending on the site of the bleeding. In approximately 60% of patients, neurologic symptoms develop gradually or stepwise over a period of hours. To some extent, the location and size of the hematoma predict clinical outcome. Headache occurs at presentation in approximately 40% of patients with ICH. Less commonly, headache develops within a few days after the ictus. Intracerebral hemorrhages presenting with headache are often located at the brain surface or within the cerebellum.
SIGNS AND SYMPTOMS Intracranial Hemorrhage Depression in the level of consciousness and vomiting occur in 50% of patients, particularly those with large cerebellar bleeds. Seizures occur at onset in up to 10% and are seen most commonly with lobar bleeds in the anterior circulation. There are rare incidences of patients with deep hemorrhages having seizures.
SIGNS AND SYMPTOMS Intracranial Hemorrhage The subsequent risk for seizures in ICH patients is up to 29% for those with lobar hemorrhages but only 4% for those with deep hemorrhages. Other symptoms seen in association with ICH include lowgrade fever without obvious infection, cardiac arrhythmias, and dysautonomia, especially with pontine bleeds.
NEUROIMAGING AND OTHER INVESTIGATIONS Routine blood tests will include FBC, U&E and LFTs. Na+ will be low due to inappropriate ADH secretion. Skull x-ray is usually done , but if pineal gland is calcified, then a shift is seen. Imaging studies include CT scan and MRI-scan are required. Both works very good but MRI is better in delineating soft tissue. A known primary tumour will exist or it can be sought out by chest x-ray or by mammography. Imaging tests will indicate the site of a lesion but usually it will not indicate the nature or whether it is a tumour or an abscess.
NEUROIMAGING Skull radiograph Pituitary fossa abnormalities. Bone density changes (e.g. tumour, meningioma, Paget’s). Position of calcified pineal
NEUROIMAGING Cranial CT Disturbances in the normal anatomy of the ventricular system. Skull base and vault. Width of cortical fissures/sulci. Midline shift. Areas of abnormal tissue density. Opacity or lucency of sinuses. Normal flow voids.
NEUROIMAGING Cranial CT High density (‘white’) signal Fresh blood. Calcification: Slow growing tumour. AVM/aneurysm. Hamartoma. In pineal/choroid plexus/basal ganglia, may be normal.
NEUROIMAGING Cranial CT Low density (‘black’) signal Infarction. Tumour. Abscess. Oedema. Encephalitis. Resolving haematoma.
NEUROIMAGING Cranial CT Mixed density Tumour. Abscess. AVM. Contusion. Haemorrhagic infarct.
NEUROIMAGING Cranial CT (After administration of IV contrast medium) Common patterns of enhancement include Ring enhancement of tumours and abscesses. Solid enhancement of meningiomas. Meningeal enhancement with meningeal disease involvement.
NEUROIMAGING Magnetic resonance imaging (MRI) In general T1 CSF is hypointense (‘black’); fat and mature blood clot white. T2 CSF is hyperintense (‘white’). MRI with enhancement (Intravenously administered gadolinium leaks through areas of damaged blood--brain barrier to give a marked enhancement) Ischaemia. Infection. Tumour (may help differentiate from surrounding oedema). Active demyelination.
NEUROIMAGING Positron Emission Tomography Form of molecular imaging that requires an injection of a radioactive tracer into the blood stream. Radionuclide tracers are prepared using a cyclotron device and a wide variety of molecules can be labelled by this means, including metabolically active substances. 18 F-fluorodeoxyglucose (FDG).
NEUROIMAGING Positron Emission Tomography Metabolic imaging technique that is capable of differentiating benign and malignant tumours more accurately. Used extensively in staging of brain tumours as it can produce a visual mapping of biochemical changes caused by the metabolic activity of the brain tumour.
Patient with a high grade Glioma tumour showing (a) T1w post contrast enhancing margins with the central area of necrosis in the tumour, (b) T2w image confirming the findings. (c) The combined PET-CT using FET tracer shows the tumour clearly with infiltrations to the cerebral cortex and infiltration to the contralateral hemisphere.
NEUROIMAGING Angiography Strongly suspected or confirmed SAH. Suspected cerebral vasculitis Delineation of other vascular abnormalities arteriovenous malformations, AVM Delineation of tumour blood supply
INVESTIGATIONS Lumbar puncture (LP) CNS Infection: Meningitis. Encephalitis/ Cerebral abscess Suspected subarachnoid haemorrhage (SAH). In general, a –ve CT does not exclude a SAH. Suspected malignancy with meningeal involvement. To seek specific antibodies/markers in CSF, Syphilis. Tumour markers.
INVESTIGATIONS Diagnostic & prognostic antibodies and other markers in blood Systemic infections Serology for many diseases PCR for TB. Disorders of coagulation: thrombophilia screen currently commonly Protein S and C levels. Antithrombin III levels. Screening for the Leiden mutation in factor V. Lupus anticoagulant. e.g. Borrelia in Lyme disease; HIV.
INVESTIGATIONS Diagnostic & prognostic antibodies and other markers in blood Tumour markers CEA for gut neoplasia (brain metastasis) Beta HCG, Alphafetoprotein in pineal tumour Endocrinopathies TSH, T4, GH, Prolactin, Cortisol in pituitary lesion
INVESTIGATIONS Neuro-otology Pure tone audiometry For lesion with the involvement of auditory meatus Acoustic neuroma CPA meningioma Neuro-ophtalmology Visual field and Visual acuity Lesion with the involvement of optic nerves, optic tract, optic radiation and visual cortex
TREATMENT Management will depends mainly on the cause of lesion. If possible, especially with primary tumours complete excision is done but this is so difficult due to infiltration and by surrounding structures. These will vary with radiosensitivity and will show response to chemotherapy. If malignancy is metastatic then treatment should include radiotherapy. However, surgery is contemplated with up to 3 metastases. Haematoma will need evacuation. Infectious lesions will need both evacuation and antibiotics.
TREATMENT Other treatments are required either as a part of radical treatment or as palliative care. Dexamethasone will reduce cerebral oedema. Mannitol will reduce raised intracranial pressure. Anticonvulsants are required but are not to be given prophylactically . Treat headache with codeine phosphate because it will avoids the pupillary effect of opiates.
TREATMENT Biopsies A biopsy should be undertaken to answer specific questions, in the light of a differential diagnosis formulated following history, examination and other investigations. Diagnosis and management of suspected primary and some metastatic brain tumours. (Tissue diagnosis) Differential diagnosis of other mass lesions (inflammatory and infective). Differentiation of radiation necrosis and tumour regrowth. Differentiation of neoplastic and non-neoplastic cysts (and their drainage). Diagnostic biopsy of a suspected infectious lesion that has not responded to a trial of therapy. Diagnosis of cerebral vasculitis or vasculopathy.
TREATMENT Surgery Cytoreduction Cytoreductive surgery for low - grade and malignant gliomas improves survival. Survival benefits for the resection of single and multiple brain metastases. Extent of resection (EOR) may be significant in determining survival for both low – grade and high grade gliomas.
TREATMENT Surgery Surgical Cure Many extra - axial tumors and some intra - axial tumors afford the neurosurgeon the opportunity for gross total resection and surgical cure. Benign tumors such as meningiomas, pituitary adenomas, cranial nerve schwannomas, chordomas, dermoids and epidermoids, choroid plexus papillomas, pilocytic astrocytomas, and hemangioblastomas may, in many cases, be cured with complete surgical resection.
TREATMENT CNS Infection Antibiotic treatment must be initiated as soon as possible, and later guided by CSF examination results. Patients must receive at least 10 days of high-dose IV antibiotics that easily cross the blood–brain barrier. Empiric IV therapy with a third-generation cephalosporin, such as ceftriaxone or cefotaxime, plus vancomycin must commence pending results of the bacterial cultures. High-dose corticosteroids, administered before antibiotic therapy, are recommended for all children and should be seriously considered for adults with community-acquired meningitis. When culture and sensitivity data are available, a specific antimicrobial therapy can be determined.
TREATMENT Brain abscesses Empiric medical therapy is started with a third- or fourthgeneration cephalosporin or penicillin plus metronidazole, depending on the setting. Brain edema associated with acute brain abscess necessitates use of steroids and mannitol, as well as phenytoin, to prevent convulsions. Patients must receive at least 4 to 6 weeks of high-dose IV antibiotics that easily cross the blood–brain barrier, followed by 2-4 weeks of oral antibiotics.
TREATMENT Brain abscesses Therapeutically, the abscess may be directly aspirated. Burrhole and drainage of abscess or craniotomy and excision of abscess may be indicated depending on the size of the abscesses and the depth from the cortical surface. Surgery may not be necessary if follow-up CT demonstrates decreased abscess size.
TREATMENT Cerebral tuberculoma PCR and CSF culture or culture of biopsied lesional material confirms the diagnosis. Because standard medical therapy is usually successful if multidrug resistance is not identified, antituberculous therapy must be attempted before surgery is contemplated. Of course, if there are signs of impending herniation, immediate surgery is indicated.
TREATMENT Intracranial Hemorrhage The initial management of ICH, after ensuring adequate ventilation and hemodynamic stability, involves correcting coagulopathies, treating hypertension, and addressing the possibility of increased intracranial pressure. In patients with intraventricular blood and early hydrocephalus, placement of a temporary external drain should be considered. Beyond these basics principles, the best treatment of ICH remains unclear and quite variable from center to center and in different countries. Although some advocate invasive techniques for hematoma evacuation, others rely mostly on medical treatment and supportive care
TREATMENT Intracranial Hemorrhage However, when a nondominant hemispheric or cerebellar ICH threatens impending herniation and before the patient’s level of consciousness significantly deteriorates, emergent surgery may be lifesaving and may provide a reasonably good recovery, especially in younger patients.
PROGNOSIS Intracranial Neoplasm Gliomas are rarely completely excised, as infiltration spreads beyond the radiologically evident boundaries of the tumour. Recurrence is therefore common, even if the tumour mass is apparently completely removed. Prognosis for benign tumours is good, provided complete surgical excision can be achieved.
PROGNOSIS Intracranial Infection Of patients with bacterial meningitis, approximately 15% experience acute and chronic complications, including various cranial nerve dysfunction, particularly those affecting extraocular function (cranial nerves III, IV, and VI), CN-VII, and sometimes CN-VIII, although this is less common today with the antibiotics lacking specific ototoxicity or vestibular toxicity. Even with early diagnosis, mortality rates are still at least 10% for meningococcal and 30% for pneumococcal meningitis.
PROGNOSIS Intracerebral hemorrhage Surgery demonstrated slightly better outcome (26.1% vs. 23.8%), but survival rates appeared to be similar in surgically and medically treated patients. The outcome from surgery likely depends on several factors, including the fact that deep-seated basal ganglia or thalamic hemorrhages are difficult to evacuate without disrupting surrounding normal structures and exacerbating brain damage, especially with open craniotomy. Patients who have small hematomas (smaller than 30 cm3) seem to do generally well without surgical evacuation. However, larger hematomas (larger than 60 cm3) do poorly, even when evacuated surgically.
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