Showing posts with label MRI. Show all posts
Showing posts with label MRI. Show all posts
Tuesday, December 9, 2008
Contrast Media Administration Guidelines by the ACR (American College of Radiology) Version 6 - 2008
Contrast Media Administration Guidelines by the ACR (American College of Radiology) Version 6 - 2008
Friday, November 21, 2008
NEURO – IMAGING IN PSYCHIATRY
NEURO – IMAGING IN PSYCHIATRY
Dr Himadri Sikhor Das
In psychiatry Neuroimaging is primarily used to aid in differential diagnosis. The clinical value of neuroimaging is used to demonstrate underlying organic brain pathology as a possible cause of disturbed mental status. Pathognomonic image profiles indicative of specific psychiatric disorders have not yet been fully identified; thus for the time being neuroimaging studies are finding only limited utility in identification of specific primary psychiatric diseases. In the future, however neuroimaging techniques may be used to make or confirm psychiatric diagnoses and neuroimaging profiles may be incorporated into the diagnostic criteria of certain psychiatric disorders. However in the future, imaging data may be valualable for predicting natural courses of illness as well as monitoring response to treatment.
MRI IMAGING IN PSYCHIATRIC ILLNESSES: -
Although specific clinical decisions must be mode on a case-to-case basis, tentative guidelines regarding the indications for structural neuroimaging in psychiatry have been suggested. These should be considered for patients who meet any of the four following criteria: -
1. Acute mental status change (including those of affect, behaviors or personality), plus any of:
- Age > 50 years
- Abnormal neurological examination.
- History of significant head trauma (i.e. Head trauma resulting in loss of consciousness or neurological sequelae)
2. New onset psychosis
3. New onset delirium or dementia of unknown etiology.
4. Prior to an initial course of ECT.
In addition to the above which focus on acute presentation; neuroimaging should also be considered when a patient’s distorted metal status proves refractory. Following these criteria a very low proportions of brain lesion associated with treatable general medical conditions could be missed. Move specifically, older age groups, psychiatric inpatients and patients with co-morbid medical illness likely will present the highest rate of positive findings. Finally an even higher percentage of patients may benefit from negative findings in a more subtle fashion i.e., as a consequence of the reassurance attained from having gross structural pathology ruled out and the primary psychiatric diagnoses solidified.
ROLE OF MRI IN CLINICAL NEUROSCIENCE: -
MRI is seen to play an important role in clinical neuroscience research in psychiatry. In general studies are done with two aims: -
- First images from large cohorts of patients and comparison subjects are reserved in order to identity pathological change that occurs in ill individuals.
- Second general research approach in to ask focused questions about the volume or shape of specific brain tissue types or structure to provide evidence regarding the involvement of these structures in the pathophysiology of specific conditions.
RECENT IMAGING MODALITIES: Recent advances in NMR and nuclear medicine techniques are finding more and more importance in pursuing active research work in Psychiatric diseases as well providing new insights into the human brain. With the advent of functional imaging, processes like memory, emotion, thought etc are being researched by scientists all over the world.
I. NUCLEAR MEDICINE (PET/SPECT):
Nuclear medicine procedures used for diagnosis and research of psychiatric conditions generally utilize PET and SPECT scans. These methods show blood flow by imaging trace amounts of radioisotopes. PET however can measure metabolism revealing how well the body is functioning. Use of radioactive tracers is well suited to studies of epilepsy, schizophrenia, Parkinson’s disease and stroke. Both PET and SPECT depict the distribution of blood into tissues, but PET does so with greater accuracy.
PET scanners watch the way the tissue cells (eg. brain cells) consume substances such as sugar (glucose). The substance is tagged with a radioisotope and brewed in a small, low energy cyclotron. The isotope has a small half-life meaning it loses half of its radioactivity only within minutes or hours of being created. Injected into the body the radioactive solution emits positrons wherever it flows. The positrons collide with electrons and the two annihilate each other releasing a burst of energy in the form of two gamma rays. These rays shoot in opposite directions and strike crystals in a ring of detectors around the patient’s head causing the crystals to light up. A computer records the location of each flash and plots the source of radiation, translating the data into an image. By tracing the radioactive substance a doctor can pinpoint areas of abnormal brain activity or determine the health of cells. Unlike PET, which specially requires a cyclotron on site, SPECT uses commercially available radioisotopes greatly reducing the cost of operation.
II. FUNCTIONAL MAGNETIC RESONANCE IMAGING (FMRI) IN PSYCHIATRY.
First, the most commonly used fMRI technique called BOLD-fMRI (Blood-Oxygen-Level-dependent fMRI) potentially offers imaging with a temporal resolution on the order of 100 milliseconds and a spatial resolution of 1-2 millimeters, which is much greater than that of PET and SPECT scanning. This means that transient cognitive events can potentially be imaged and small structures like the amygdala can be more readily resolved. Most fMRI techniques are noninvasive and do not involve the injection of radioactive materials so that a person can be imaged repeatedly. This allows imaging of a patient repeatedly through different disease states (i.e. imaging a bipolar patient through manic, depressive, and euthymic states) or developmental changes (ie. Learning cognitive stages of development, stages of grief recovery). Third, with fMRI, one can easily make statistical statements in comparing different mental states within an individual in a single session. Thus, fMRI may be of important use in understanding how a given individual’s brain functions and perhaps, in the future, making psychiatric diagnoses and treatment recommendations. It is in fact already starting to being used in presurgical planning to map vital areas like languages, motor function, and memory.
The four main applications of MRI yielding functional information in psychiatry can be categorized as: -
1. BOLD-fMRI that measures regional differences in oxygenated blood.
2. Perfusion fMRI, which measures regional cerebral blood flow.
3. Diffusion-weighted fMRI which measures random movement of water molecules and
4. MRI spectroscopy, which can measure certain cerebral metabolites noninvasively.
1. BOLD-fMRI (BLOOD-OXYGEN-LEVEL-DEPENDENT FMRI):
BOLD-fMRI is currently the most common fMRI technique. With this technique, it is assumed that an area is relatively more active when it has more oxygenated blood compared to another point in time. This is based on the principle that when a brain region is being used, arterial oxygenated blood will redistribute and increase to this area. BOLD fMRI is a relative technique in that it must compare images taken during one mental state to another to create a meaningful picture. As images are acquired very rapidly (ie. a set of 15 coronal brain slices every 3 seconds is commonly) one can acquire enough images to measure the relative differences between two states to perform a statistical analysis within a single individual. Ideally, these states would differ in only one aspect so that everything is controlled for except the behavior in question.
BOLD fMRI paradigms generally have several periods of rest alternating with several periods of activation. Images are then compared over the entire activation to the rest periods. BOLD fMRI is best used for studying processes that can be rapidly turned on and off like language, vision, movement, hearing and memory.
BOLD fMRI is very sensitive to movement so that tasks are limited to those without head movement, including speaking. BOLD fMRI is also limited in that artifacts are often present in brain regions that are close to air (ie. sinuses). Thus there are some problems in observing important emotional regions at the base of the brain like the orbitofrontal and medial temporal cortices. Another problem is that sometimes observed areas of activation may be located more in areas near large draining veins rather than directly at a capillary bed near the site of neuronal activation.
Currently, there are no indications for BOLD fMRI in clinical psychiatry, although this technique holds considerable promise for unraveling the neuroanatomic basis of psychiatric disease. It may be of potential help in sorting out diagnostic heterogeneity and treatment planning in the future. Neurologists and neurosurgeons are beginning to use this technique clinically to noninvasively map language, motor and memory function in patients undergoing neurosurgery.
2. PERFUSION fMRI:
Two fMRI methods have been developed for measuring cerebral blood flow. The first method, called intravenous bolus tracking, relies on the intravenous (iv) injection of a magnetic compound such as a gadolinium-containing contrast agent and measuring its T2 weighted signal as it perfuses through the brain over a short time period of time.
Areas perfused with the magnetic compound show less signal intensity as the compound creates a magnetic inhomogeneity that decreases the T2 signal. The magnetic compound may be injected once during the control and once during the activation task and relative differences in blood flow between the two states may be determined to develop a perfusion image. Alternatively one can measure changes in blood few over time over time after a single injection to generate a perfusion map.
This technique also only generates a map of relative cerebral blood flow, not absolute flow as in the text technique. Arterial spin labeling is a T1 weighted noninvasive technique where intrinsic hydrogen atoms in arterial water outside of the slice of interest are magnetically tagged (“flipped”) as they course through the blood and are then imaged as they enter the slice of interest.
Arterial spin labelling is noninvasive, does not involve an IV bolus injection, and can, thus, be repeatedly performed in individual subjects. Also, absolute regional blood flow can be measured which cannot be easily measured with SPECT or BOLD fMRI and requires an arterial line with PET. As absolute information is obtained, cerebral blood flow can be serially measured over separate imaging sessions such as measuring blood flow in bipolar subjects as they course through different disease states. Absolute blood flow information may be important in imaging such processes as anxiety, which may be hard to turn on and off. For instance, in social phobics, a relaxation task may be imaged on one day and anticipating making a speech may be imaged on the next day. Comparing these separate tasks in different imaging sessions would not be possible with BOLD fMRI. Arterial spin labelling has some limitations in that it takes several minutes to acquire information on a single slice of interest. Therefore, one must have a specific brain region that one is interested in examining. Also, as it currently takes several minutes to acquire a single slice, it would be tedious obtaining enough images on this slice within a single session to make a statistical statement on a given subject.
3. DIFFUSION-WEIGHTED IMAGING (DWI)
Diffusion-weighted imaging is very sensitive to the random movement of 1 H in water molecules (Brownian movement). The amount of water diffusion for a given pixel can be calculated and is called the apparent diffusion coefficient (ADC). Areas with low ADC value (ie. low diffusion) appear more intense. ADC values are direction sensitive. While it is currently unclear now diffusion-weighted imaging will be useful in studying psychiatric disorders, it hold great promise for changing the clinical management of acute ischaemic stroke by potentially refining the criteria for patients most likely to benefit from thrombolytic therapy.
4. MRI SPECTROSCOPY (MRS):
MRI spectroscopy (MRS) offers the capability of using MRI to noninvasively study tissue biochemistry. In the conventional and functional MRI techniques listed. The hydrogen atom in water is the main one that is flipped (resonated). In MRS, either 1H atoms in other molecules or other atoms such as 31P, 23Na, K, 19F or Li are flipped. Within a given brain region called a voxel, information on these molecules is usually presented as a spectrograph with precession frequency on the x-axis revealing the identity of a compound and intensity on the y-axis, which helps quantify the amount of a substance. The quantity of a substance is related is related to the area under its spectrographic peak; the larger the area, the more of a substance that is present.
The two most widely used MRS techniques involve either viewing 1H atoms in molecules other than water or 31P-containing molecules. In 1H MRS, the water signal must first be suppressed as it is much greater than the signal from other 1H-containing compounds and has overlapping spectroscopic peaks with compounds.
Compounds that can be resolved with 1H-MRS include:
a) N-acetylaspartate (NAA) which is though to be a neuronal marker that decreases in processes where neurons die;
b) Lactate which is a product of anaerobic metabolism and may indicate hypoxia;
c) Excitatory neurotransmitters glutamate and aspartate;
d) The inhibitory neurotransmitter gamma-amino butyric acid (GABA);
e) Cytosolic choline which includes primarily mobile molecules involved in phospholipid membrane metabolism but also small amounts of the neurotransmitter acetylcholine and its precursor choline;
1. Myolinositol which is important in phospholipoid metabolism and intracellular second messenger systems; and
2. Creatine molecules such as creatine and phosphocreatine, which usually have relatively constant concentrations throughout the brain and are often used as relative reference molecules (ie. one may see NAA concentration reported as the ratio NAA/creatine in the literature).
Phosphorus (31P) MRS allows the quantification of ATP metabolism, intracellular pH, and phospholipid metabolism. Mobile phospholipid, including phosphomonoesters (PME - putative cell membrane building blocks) and phosphodiesters (PDE – putative cell membrane breakdown products) can also be measured, supplying information on phospholipid membrane metabolism.
MRS can be used to identify regional biochemical abnormalities. For example, P-MRS studies of euthymic bipolar patients have revealed decreased frontal lobe PMEs (cell membrane building blocks) compared with healthy controls. However, when bipolar patients become either manic or depressed, their PMEs increase.
These findings appear to be unrelated to medication treatment. The finding of decreased frontal PMEs in euthymic bipolars has also been demonstrated in schizophrenia and speculatively accounts for the finding of decreased frontal lobe metabolism in both of these disorders. The schizophrenia finding also appears to be medication-independent.
MRS may also be of future help in the differential diagnosis of certain psychiatric diseases such as dementia. In normal aging, there is a decrease in PMEs and increase in PDEs. In early Alzheimer’s Dementia compared with healthy controls. Some believe that a decrease in NAA coupled with an increased myoinositol lever helps in differentiating probable Alzheimer’s Dementia from healthy age-matched controls as well as other dementias (usually decreased NAA but normal myoinositol levels).
With MRS, changes in metabolic activity can be measured over time within an individual scanning session. MRS can also be used to measure changes in metabolic activity between sessions, such as before and after medication treatment. For example, Satlin et al. (1997) used 1H MRS to measure midparietal lobe cytosolic choline levels in 12 Alzheimer’s subjects before and after treatment with Xanomeline, an M1 selective cholinergic agonist, or placebo. Additionally, MRS can be used to measure drug levels of certain psychotropic drugs. The magnetic elements Li and F do not naturally occur in the human body but they are fund in psychotropic drugs; lithum for Li and fluoxetine and stelazine for F. For example, studies have consistently found that the brain concentrations of lithium are about 0.5 that of serum Li levels and correlate with treatment response.
For psychiatry, MRS is a research to be used in the characterization of tumor, stroke and epileptogenic tissue and in presurgical planning.
LIMITATIONS:
MRS is restricted to studying mobile magnetic compounds. As neurochemical receptors are noted usually mobile, they cannot be measured with MRS. Thus, receptor-ligand studies are still the domain of SPECT and PET. Another problem with MRS is that due to the low concentrations of many of the imaged substances, larger areas than with water are needed to obtain detectable signals. Larger volume units imaged over longer periods are thus used with this technique, limiting both temporal and spatial resolution compared with conventional MRI and BOLD-fMRI. However, stronger magnetic fields which can spread out precession frequencies over a wider range may improve this resolution.
A brief view of recent findings are outlined.
PSYCHOTIC DISORDERS:
Research studies have identified a large number of pathologies in at last some subjects of schizophrenia for eg, the main regions sharing consistent abnormalities in schizophrenia have been frontal & temporal lobe structures. Volume decreases have been found in 62% of 37 studies of the whole temporal lobe, in 81% of 16 studies of the superior temporal gyrus and in 77% of 30 studies of the medial temporal lobe. Temporal lobe volume reduction may be uni or bilateral with deficits observed more commonly in left temporal lobe. Frontal lobe volume reductions have been reported in 55% of all published studies. Regional volume reductions have been reported in thalamus and corpus callosum. Interestingly, basal ganglia volumes may increase during treatment with typical, but not atypical neuroleptic agents. Recently studies in children have also shown findings consistent with the adult findings.
MOOD DISORDERS:
Major Depression
The spectrum of affective illness is very broad, ranging from single episodes of depressed mood, which are self-limited to life-long, treatment-refractory despondency with recurrent suicidality. Proposed that both primary and secondary mood disorders may involve abnormalities in specific frontosubcortical circuits that regulate mood. Depression is observed frequently in persons with degenerative diseases of the basal ganglia, such as Huntington’s disease, Parkinson’s disease, Wilson’s disease.
In older adults, frontal lobe atrophy and an increasing burden of T2 weighted, high signal intensity lesions have been correlated with late-life depression. Evidence suggests that depression may be seen following focal damage to critical brain regions as well as in response to diffuse brain injury. As the amygdala plays a key role in the brain’s integration of emotional meaning with perception and experience, volumetric studies of this brain structure currently are being reported. Sheline et al. have observed decreased amygdalar core nuclei volumes in depressed subjects increased amygdalar volumes in depressed patients. Mervaala et al. have noted significant amygdalar asymmetry (right smaller than left) in severely depressed subjects.
Strokes and tumors located in left sided frontal regions have been associated with new onset depression and less commonly; right-sided lesions may lead to manic symptoms. Subcortical lesions, especially of the caudate and thalamus, also can lead to mood dysregulation, with right sided lesions again being more commonly associated with mania. 30 MR studies with most consistent finding observed in 10 of 12 studies is a three-fold increase in the presence of WMH. The etiology of these WMH in bipolar patients is not clear, rates of alcohol and substance abuse, smoking cardiovascular risk factors contribute. As in schizophrenia some patients with bipolar disorder have increased lateral and third ventricular volume. Brain regions with volume deficits in bipolar include the cerebellum, especially in patients who are older or how have had multiple episodes of mania toxic effects of alcohol abuse lithium treatment.
Reduced volume and altered activity of subgenual prefrontal cortex in familial bipolar disorder has been reported. Subgenual cingulate cortex volume more recently increased amygdalar volumes have been seen in persons with bipolar disorder. Limited available data suggest that panic attacks may arise, in a minority of cases, as a consequence of ictal activity and that brain MR may identify a reasonably high yield of septo-hippocampal abnormalities in the subpopulation of panic patients who also have electroencephalogram abnormalities. Emission tomography studies generally have observed increased orbitofrontal and cingulate blood flow and glucose utilization, with decreased caudate perfusion. Hippocampal volume reductions on the order of 5% to 12% have been reported, which are of a lesser magnitude than those observed in AD or temporal-lobe epilepsy.
Neuroimaging studies of Dementing illness constitute a very active area of ongoing research. A great deal of attention has been paid to the hippocampus, as progressive atrophy has been reported to correlate with memory loss in a number of studies of both healthy adults and individuals with dementing illnesses. Recently have suggested that other regions of interest (e.g. entorhinal cortex, anterior cingulate and the banks of the superior temporal sulcus) may show larger rates of change in structural volume, over the for the hippocampal formation. Assessment of the medial occipitemporal, inferior and middle temporal gyri in demented elderly also has been suggested as a means to predict progression to AD. Alternatively, measurement of global cerebral volume also has been proposed as a means to assess disease progression. In healthy older adults, ventricular volume has been shown to increase by approximately 1.5 cm / year, suggesting that brain tissue loss is relatively slow in the absence of degenerative disorders. Frontotemporal dementia (FTD) may be distinguished from AD on the basis of anterior hippocampal atrophy (AD).
Decreases in the area of the body and posterior subregions of the corpus callosum have been reported in autistic individuals. Anorexia nervosa has been strongly associated with cerebral ventricular enlargement as well as gray and white matter deficits. Refeeding is associated with some improvement in ventricular and white matter volumes but gray matter volume deficits tend to persist, as do some neurocognitive impairments. Anorexia and bulimia may be associated with hyponatremia, which can lead to the development of central pontine myelinolysis.
Substance Use Disorders.
Alcohol-induced ventricular and sulcal enlargement have been observed by many. Regional atrophy of the corpus callosum and the hippocampus also have been reported. The cerebellum appears to be particularly sensitive to alcohol-induced damage. In addition to atrophic changes, diffuse white matter hyperintensities, suggestive of demyelination have been observed in T2 weighted examination of asymptomatic alcoholics. Signal intensity changes within the globus pallidus also have been observed in persons with cirrhosis, which may improve following liver transplantation.
Wernicke korsakoff syndrome results from nutritional deficiencies and may be precipitated by glucose administration to thiamine deficient alcoholics. The neuroanatomic change most closely associated with Wernicke Korsakoff syndrome in mamillary body atrophy although regional changes in the thalamus, orbitofrontal cortex and mesial temporal lobe also have been reported. Central pontine myelinolysis often is detected in alcoholics and presumably arises from rapid correction of electrolyte imbalance in severe hyponatremia. Extrapontine lesions also may be observed in CPM patient, affecting the cerebellar peduncles, basal ganglia and the thalamus. Marchiafava Bignami disease is a rare hemispheric disconnection syndrome typically associated with chronic alcoholism. MBD often is associated with hypointense T1 weighted or hyperintense T2 weighted lesions of the corpus callosum, suggestive of demyelination. Alcohol discontinuation and nutritional supplementation may contribute to recovery from MBD.
Stimulant Dependence.
Cocaine dependence recently has been associated with an increased incidence of WMH on T2 weighted imaging studies an incidence rate for asymptomatic stroke of approximately 3% in abstinent former cocaine users. Abuse of amphetamine and methampetamine also have been associated with cerebral ischaemia.
Other Drugs
Lipophilic adulterants present in preparations of vaporized heroin may produce signs of a toxic leukoencephalopathy. Chronic use of combined heroin and cocaine has been associated with increased pituitary volume as well as reduced prefrontal and temporal cortex volume. Solvent abuse has been linked to loss of gray white matter tissue differentiation, increased perivascular white-matter signal hyperintensities and cerebral atrophy.
CONCLUSIONS:
While there are currently no clinical indications for ordering any of these fMRI techniques, they hold considerable promise for unraveling the neurocircuitry and metabolic pathways of psychiatric disorders in the immediate future and in further helping in psychiatric diagnosis and treatment planning.
REFERENCES:
1. Magnetic resonance imaging of Brain and spine, Third Edition, Volume – I, 2002, chapter 22, Page no = 1189-1205
2. Posse S, Muller-Gartner HW, Dager SR. Functional Magnetic Resonance Studies of Brain Activation. Seminars in Clinical neuropsychiatry 1996; 1:76-88.
3. Bonder JR, Swanson SJ, Hammeke TA Morris GL, Myeller WM, Fischer M, et al. Determination of language dominance using functional MRI: A comparison with the Wada test. Neurol 1996; 46:978-984.
4. Moseley ME, Decrespigny A, Spielman DM. Magnetic Resonance Imaging of Human Brain Function. Surgical neurology 1996; 45:385-391.
5. David A, Blamire A, Breiter H. Functional Magnetic Resonance Imaging: A new technique with implications for psychology and psychiatry. Brit J Psychiatry 1994: 164:2-7.
6. Menon RS, Ogawa S, Hu X, Strupp JP, Anderson P, Ugurbil K. BOLD based functional MRI at 4 Tesla includes a capillary bed contribution: echo-planar imaging correlates with previous optical imaging using intrinsic signals. Magn Res Med 1995; 33: 453-459
7. Belliveau JW, Kennedy DN, McKinstry RC, Buchbinder BR, weisskoff RM, Cohen MS, et al. Functional mapping of the visual cortex by MRI. Science 1991; 254: 716-719.
8. Harris GJ Lewis RF, Satlin A, English CD, Scott TM et al. Dynamic susceptibility contrast MRI of regional cerebral blood volume in Alzheimer’s disease. Am J psychiatry 1996; 153: 721-724
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10. Zivan JA. Diffusion-weighted MRI for diagnosis and treatment of ischaemic stroke. Ann neurol 1997;567-568
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12. Frangou S, Williams SC. Magnetic resonance spectroscopy in psychiatry: Basic principles and applications. British Medical Bulletin 1996 ; 52:474-485
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14. Functional magnetic resonance imaging (fMRI) for the pshychiatrist Lorberbaum JP, Bohning DE, Shastri A, Nahas Z et al.
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Dr Himadri Sikhor Das
In psychiatry Neuroimaging is primarily used to aid in differential diagnosis. The clinical value of neuroimaging is used to demonstrate underlying organic brain pathology as a possible cause of disturbed mental status. Pathognomonic image profiles indicative of specific psychiatric disorders have not yet been fully identified; thus for the time being neuroimaging studies are finding only limited utility in identification of specific primary psychiatric diseases. In the future, however neuroimaging techniques may be used to make or confirm psychiatric diagnoses and neuroimaging profiles may be incorporated into the diagnostic criteria of certain psychiatric disorders. However in the future, imaging data may be valualable for predicting natural courses of illness as well as monitoring response to treatment.
MRI IMAGING IN PSYCHIATRIC ILLNESSES: -
Although specific clinical decisions must be mode on a case-to-case basis, tentative guidelines regarding the indications for structural neuroimaging in psychiatry have been suggested. These should be considered for patients who meet any of the four following criteria: -
1. Acute mental status change (including those of affect, behaviors or personality), plus any of:
- Age > 50 years
- Abnormal neurological examination.
- History of significant head trauma (i.e. Head trauma resulting in loss of consciousness or neurological sequelae)
2. New onset psychosis
3. New onset delirium or dementia of unknown etiology.
4. Prior to an initial course of ECT.
In addition to the above which focus on acute presentation; neuroimaging should also be considered when a patient’s distorted metal status proves refractory. Following these criteria a very low proportions of brain lesion associated with treatable general medical conditions could be missed. Move specifically, older age groups, psychiatric inpatients and patients with co-morbid medical illness likely will present the highest rate of positive findings. Finally an even higher percentage of patients may benefit from negative findings in a more subtle fashion i.e., as a consequence of the reassurance attained from having gross structural pathology ruled out and the primary psychiatric diagnoses solidified.
ROLE OF MRI IN CLINICAL NEUROSCIENCE: -
MRI is seen to play an important role in clinical neuroscience research in psychiatry. In general studies are done with two aims: -
- First images from large cohorts of patients and comparison subjects are reserved in order to identity pathological change that occurs in ill individuals.
- Second general research approach in to ask focused questions about the volume or shape of specific brain tissue types or structure to provide evidence regarding the involvement of these structures in the pathophysiology of specific conditions.
RECENT IMAGING MODALITIES: Recent advances in NMR and nuclear medicine techniques are finding more and more importance in pursuing active research work in Psychiatric diseases as well providing new insights into the human brain. With the advent of functional imaging, processes like memory, emotion, thought etc are being researched by scientists all over the world.
I. NUCLEAR MEDICINE (PET/SPECT):
Nuclear medicine procedures used for diagnosis and research of psychiatric conditions generally utilize PET and SPECT scans. These methods show blood flow by imaging trace amounts of radioisotopes. PET however can measure metabolism revealing how well the body is functioning. Use of radioactive tracers is well suited to studies of epilepsy, schizophrenia, Parkinson’s disease and stroke. Both PET and SPECT depict the distribution of blood into tissues, but PET does so with greater accuracy.
PET scanners watch the way the tissue cells (eg. brain cells) consume substances such as sugar (glucose). The substance is tagged with a radioisotope and brewed in a small, low energy cyclotron. The isotope has a small half-life meaning it loses half of its radioactivity only within minutes or hours of being created. Injected into the body the radioactive solution emits positrons wherever it flows. The positrons collide with electrons and the two annihilate each other releasing a burst of energy in the form of two gamma rays. These rays shoot in opposite directions and strike crystals in a ring of detectors around the patient’s head causing the crystals to light up. A computer records the location of each flash and plots the source of radiation, translating the data into an image. By tracing the radioactive substance a doctor can pinpoint areas of abnormal brain activity or determine the health of cells. Unlike PET, which specially requires a cyclotron on site, SPECT uses commercially available radioisotopes greatly reducing the cost of operation.
II. FUNCTIONAL MAGNETIC RESONANCE IMAGING (FMRI) IN PSYCHIATRY.
First, the most commonly used fMRI technique called BOLD-fMRI (Blood-Oxygen-Level-dependent fMRI) potentially offers imaging with a temporal resolution on the order of 100 milliseconds and a spatial resolution of 1-2 millimeters, which is much greater than that of PET and SPECT scanning. This means that transient cognitive events can potentially be imaged and small structures like the amygdala can be more readily resolved. Most fMRI techniques are noninvasive and do not involve the injection of radioactive materials so that a person can be imaged repeatedly. This allows imaging of a patient repeatedly through different disease states (i.e. imaging a bipolar patient through manic, depressive, and euthymic states) or developmental changes (ie. Learning cognitive stages of development, stages of grief recovery). Third, with fMRI, one can easily make statistical statements in comparing different mental states within an individual in a single session. Thus, fMRI may be of important use in understanding how a given individual’s brain functions and perhaps, in the future, making psychiatric diagnoses and treatment recommendations. It is in fact already starting to being used in presurgical planning to map vital areas like languages, motor function, and memory.
The four main applications of MRI yielding functional information in psychiatry can be categorized as: -
1. BOLD-fMRI that measures regional differences in oxygenated blood.
2. Perfusion fMRI, which measures regional cerebral blood flow.
3. Diffusion-weighted fMRI which measures random movement of water molecules and
4. MRI spectroscopy, which can measure certain cerebral metabolites noninvasively.
1. BOLD-fMRI (BLOOD-OXYGEN-LEVEL-DEPENDENT FMRI):
BOLD-fMRI is currently the most common fMRI technique. With this technique, it is assumed that an area is relatively more active when it has more oxygenated blood compared to another point in time. This is based on the principle that when a brain region is being used, arterial oxygenated blood will redistribute and increase to this area. BOLD fMRI is a relative technique in that it must compare images taken during one mental state to another to create a meaningful picture. As images are acquired very rapidly (ie. a set of 15 coronal brain slices every 3 seconds is commonly) one can acquire enough images to measure the relative differences between two states to perform a statistical analysis within a single individual. Ideally, these states would differ in only one aspect so that everything is controlled for except the behavior in question.
BOLD fMRI paradigms generally have several periods of rest alternating with several periods of activation. Images are then compared over the entire activation to the rest periods. BOLD fMRI is best used for studying processes that can be rapidly turned on and off like language, vision, movement, hearing and memory.
BOLD fMRI is very sensitive to movement so that tasks are limited to those without head movement, including speaking. BOLD fMRI is also limited in that artifacts are often present in brain regions that are close to air (ie. sinuses). Thus there are some problems in observing important emotional regions at the base of the brain like the orbitofrontal and medial temporal cortices. Another problem is that sometimes observed areas of activation may be located more in areas near large draining veins rather than directly at a capillary bed near the site of neuronal activation.
Currently, there are no indications for BOLD fMRI in clinical psychiatry, although this technique holds considerable promise for unraveling the neuroanatomic basis of psychiatric disease. It may be of potential help in sorting out diagnostic heterogeneity and treatment planning in the future. Neurologists and neurosurgeons are beginning to use this technique clinically to noninvasively map language, motor and memory function in patients undergoing neurosurgery.
2. PERFUSION fMRI:
Two fMRI methods have been developed for measuring cerebral blood flow. The first method, called intravenous bolus tracking, relies on the intravenous (iv) injection of a magnetic compound such as a gadolinium-containing contrast agent and measuring its T2 weighted signal as it perfuses through the brain over a short time period of time.
Areas perfused with the magnetic compound show less signal intensity as the compound creates a magnetic inhomogeneity that decreases the T2 signal. The magnetic compound may be injected once during the control and once during the activation task and relative differences in blood flow between the two states may be determined to develop a perfusion image. Alternatively one can measure changes in blood few over time over time after a single injection to generate a perfusion map.
This technique also only generates a map of relative cerebral blood flow, not absolute flow as in the text technique. Arterial spin labeling is a T1 weighted noninvasive technique where intrinsic hydrogen atoms in arterial water outside of the slice of interest are magnetically tagged (“flipped”) as they course through the blood and are then imaged as they enter the slice of interest.
Arterial spin labelling is noninvasive, does not involve an IV bolus injection, and can, thus, be repeatedly performed in individual subjects. Also, absolute regional blood flow can be measured which cannot be easily measured with SPECT or BOLD fMRI and requires an arterial line with PET. As absolute information is obtained, cerebral blood flow can be serially measured over separate imaging sessions such as measuring blood flow in bipolar subjects as they course through different disease states. Absolute blood flow information may be important in imaging such processes as anxiety, which may be hard to turn on and off. For instance, in social phobics, a relaxation task may be imaged on one day and anticipating making a speech may be imaged on the next day. Comparing these separate tasks in different imaging sessions would not be possible with BOLD fMRI. Arterial spin labelling has some limitations in that it takes several minutes to acquire information on a single slice of interest. Therefore, one must have a specific brain region that one is interested in examining. Also, as it currently takes several minutes to acquire a single slice, it would be tedious obtaining enough images on this slice within a single session to make a statistical statement on a given subject.
3. DIFFUSION-WEIGHTED IMAGING (DWI)
Diffusion-weighted imaging is very sensitive to the random movement of 1 H in water molecules (Brownian movement). The amount of water diffusion for a given pixel can be calculated and is called the apparent diffusion coefficient (ADC). Areas with low ADC value (ie. low diffusion) appear more intense. ADC values are direction sensitive. While it is currently unclear now diffusion-weighted imaging will be useful in studying psychiatric disorders, it hold great promise for changing the clinical management of acute ischaemic stroke by potentially refining the criteria for patients most likely to benefit from thrombolytic therapy.
4. MRI SPECTROSCOPY (MRS):
MRI spectroscopy (MRS) offers the capability of using MRI to noninvasively study tissue biochemistry. In the conventional and functional MRI techniques listed. The hydrogen atom in water is the main one that is flipped (resonated). In MRS, either 1H atoms in other molecules or other atoms such as 31P, 23Na, K, 19F or Li are flipped. Within a given brain region called a voxel, information on these molecules is usually presented as a spectrograph with precession frequency on the x-axis revealing the identity of a compound and intensity on the y-axis, which helps quantify the amount of a substance. The quantity of a substance is related is related to the area under its spectrographic peak; the larger the area, the more of a substance that is present.
The two most widely used MRS techniques involve either viewing 1H atoms in molecules other than water or 31P-containing molecules. In 1H MRS, the water signal must first be suppressed as it is much greater than the signal from other 1H-containing compounds and has overlapping spectroscopic peaks with compounds.
Compounds that can be resolved with 1H-MRS include:
a) N-acetylaspartate (NAA) which is though to be a neuronal marker that decreases in processes where neurons die;
b) Lactate which is a product of anaerobic metabolism and may indicate hypoxia;
c) Excitatory neurotransmitters glutamate and aspartate;
d) The inhibitory neurotransmitter gamma-amino butyric acid (GABA);
e) Cytosolic choline which includes primarily mobile molecules involved in phospholipid membrane metabolism but also small amounts of the neurotransmitter acetylcholine and its precursor choline;
1. Myolinositol which is important in phospholipoid metabolism and intracellular second messenger systems; and
2. Creatine molecules such as creatine and phosphocreatine, which usually have relatively constant concentrations throughout the brain and are often used as relative reference molecules (ie. one may see NAA concentration reported as the ratio NAA/creatine in the literature).
Phosphorus (31P) MRS allows the quantification of ATP metabolism, intracellular pH, and phospholipid metabolism. Mobile phospholipid, including phosphomonoesters (PME - putative cell membrane building blocks) and phosphodiesters (PDE – putative cell membrane breakdown products) can also be measured, supplying information on phospholipid membrane metabolism.
MRS can be used to identify regional biochemical abnormalities. For example, P-MRS studies of euthymic bipolar patients have revealed decreased frontal lobe PMEs (cell membrane building blocks) compared with healthy controls. However, when bipolar patients become either manic or depressed, their PMEs increase.
These findings appear to be unrelated to medication treatment. The finding of decreased frontal PMEs in euthymic bipolars has also been demonstrated in schizophrenia and speculatively accounts for the finding of decreased frontal lobe metabolism in both of these disorders. The schizophrenia finding also appears to be medication-independent.
MRS may also be of future help in the differential diagnosis of certain psychiatric diseases such as dementia. In normal aging, there is a decrease in PMEs and increase in PDEs. In early Alzheimer’s Dementia compared with healthy controls. Some believe that a decrease in NAA coupled with an increased myoinositol lever helps in differentiating probable Alzheimer’s Dementia from healthy age-matched controls as well as other dementias (usually decreased NAA but normal myoinositol levels).
With MRS, changes in metabolic activity can be measured over time within an individual scanning session. MRS can also be used to measure changes in metabolic activity between sessions, such as before and after medication treatment. For example, Satlin et al. (1997) used 1H MRS to measure midparietal lobe cytosolic choline levels in 12 Alzheimer’s subjects before and after treatment with Xanomeline, an M1 selective cholinergic agonist, or placebo. Additionally, MRS can be used to measure drug levels of certain psychotropic drugs. The magnetic elements Li and F do not naturally occur in the human body but they are fund in psychotropic drugs; lithum for Li and fluoxetine and stelazine for F. For example, studies have consistently found that the brain concentrations of lithium are about 0.5 that of serum Li levels and correlate with treatment response.
For psychiatry, MRS is a research to be used in the characterization of tumor, stroke and epileptogenic tissue and in presurgical planning.
LIMITATIONS:
MRS is restricted to studying mobile magnetic compounds. As neurochemical receptors are noted usually mobile, they cannot be measured with MRS. Thus, receptor-ligand studies are still the domain of SPECT and PET. Another problem with MRS is that due to the low concentrations of many of the imaged substances, larger areas than with water are needed to obtain detectable signals. Larger volume units imaged over longer periods are thus used with this technique, limiting both temporal and spatial resolution compared with conventional MRI and BOLD-fMRI. However, stronger magnetic fields which can spread out precession frequencies over a wider range may improve this resolution.
A brief view of recent findings are outlined.
PSYCHOTIC DISORDERS:
Research studies have identified a large number of pathologies in at last some subjects of schizophrenia for eg, the main regions sharing consistent abnormalities in schizophrenia have been frontal & temporal lobe structures. Volume decreases have been found in 62% of 37 studies of the whole temporal lobe, in 81% of 16 studies of the superior temporal gyrus and in 77% of 30 studies of the medial temporal lobe. Temporal lobe volume reduction may be uni or bilateral with deficits observed more commonly in left temporal lobe. Frontal lobe volume reductions have been reported in 55% of all published studies. Regional volume reductions have been reported in thalamus and corpus callosum. Interestingly, basal ganglia volumes may increase during treatment with typical, but not atypical neuroleptic agents. Recently studies in children have also shown findings consistent with the adult findings.
MOOD DISORDERS:
Major Depression
The spectrum of affective illness is very broad, ranging from single episodes of depressed mood, which are self-limited to life-long, treatment-refractory despondency with recurrent suicidality. Proposed that both primary and secondary mood disorders may involve abnormalities in specific frontosubcortical circuits that regulate mood. Depression is observed frequently in persons with degenerative diseases of the basal ganglia, such as Huntington’s disease, Parkinson’s disease, Wilson’s disease.
In older adults, frontal lobe atrophy and an increasing burden of T2 weighted, high signal intensity lesions have been correlated with late-life depression. Evidence suggests that depression may be seen following focal damage to critical brain regions as well as in response to diffuse brain injury. As the amygdala plays a key role in the brain’s integration of emotional meaning with perception and experience, volumetric studies of this brain structure currently are being reported. Sheline et al. have observed decreased amygdalar core nuclei volumes in depressed subjects increased amygdalar volumes in depressed patients. Mervaala et al. have noted significant amygdalar asymmetry (right smaller than left) in severely depressed subjects.
Strokes and tumors located in left sided frontal regions have been associated with new onset depression and less commonly; right-sided lesions may lead to manic symptoms. Subcortical lesions, especially of the caudate and thalamus, also can lead to mood dysregulation, with right sided lesions again being more commonly associated with mania. 30 MR studies with most consistent finding observed in 10 of 12 studies is a three-fold increase in the presence of WMH. The etiology of these WMH in bipolar patients is not clear, rates of alcohol and substance abuse, smoking cardiovascular risk factors contribute. As in schizophrenia some patients with bipolar disorder have increased lateral and third ventricular volume. Brain regions with volume deficits in bipolar include the cerebellum, especially in patients who are older or how have had multiple episodes of mania toxic effects of alcohol abuse lithium treatment.
Reduced volume and altered activity of subgenual prefrontal cortex in familial bipolar disorder has been reported. Subgenual cingulate cortex volume more recently increased amygdalar volumes have been seen in persons with bipolar disorder. Limited available data suggest that panic attacks may arise, in a minority of cases, as a consequence of ictal activity and that brain MR may identify a reasonably high yield of septo-hippocampal abnormalities in the subpopulation of panic patients who also have electroencephalogram abnormalities. Emission tomography studies generally have observed increased orbitofrontal and cingulate blood flow and glucose utilization, with decreased caudate perfusion. Hippocampal volume reductions on the order of 5% to 12% have been reported, which are of a lesser magnitude than those observed in AD or temporal-lobe epilepsy.
Neuroimaging studies of Dementing illness constitute a very active area of ongoing research. A great deal of attention has been paid to the hippocampus, as progressive atrophy has been reported to correlate with memory loss in a number of studies of both healthy adults and individuals with dementing illnesses. Recently have suggested that other regions of interest (e.g. entorhinal cortex, anterior cingulate and the banks of the superior temporal sulcus) may show larger rates of change in structural volume, over the for the hippocampal formation. Assessment of the medial occipitemporal, inferior and middle temporal gyri in demented elderly also has been suggested as a means to predict progression to AD. Alternatively, measurement of global cerebral volume also has been proposed as a means to assess disease progression. In healthy older adults, ventricular volume has been shown to increase by approximately 1.5 cm / year, suggesting that brain tissue loss is relatively slow in the absence of degenerative disorders. Frontotemporal dementia (FTD) may be distinguished from AD on the basis of anterior hippocampal atrophy (AD).
Decreases in the area of the body and posterior subregions of the corpus callosum have been reported in autistic individuals. Anorexia nervosa has been strongly associated with cerebral ventricular enlargement as well as gray and white matter deficits. Refeeding is associated with some improvement in ventricular and white matter volumes but gray matter volume deficits tend to persist, as do some neurocognitive impairments. Anorexia and bulimia may be associated with hyponatremia, which can lead to the development of central pontine myelinolysis.
Substance Use Disorders.
Alcohol-induced ventricular and sulcal enlargement have been observed by many. Regional atrophy of the corpus callosum and the hippocampus also have been reported. The cerebellum appears to be particularly sensitive to alcohol-induced damage. In addition to atrophic changes, diffuse white matter hyperintensities, suggestive of demyelination have been observed in T2 weighted examination of asymptomatic alcoholics. Signal intensity changes within the globus pallidus also have been observed in persons with cirrhosis, which may improve following liver transplantation.
Wernicke korsakoff syndrome results from nutritional deficiencies and may be precipitated by glucose administration to thiamine deficient alcoholics. The neuroanatomic change most closely associated with Wernicke Korsakoff syndrome in mamillary body atrophy although regional changes in the thalamus, orbitofrontal cortex and mesial temporal lobe also have been reported. Central pontine myelinolysis often is detected in alcoholics and presumably arises from rapid correction of electrolyte imbalance in severe hyponatremia. Extrapontine lesions also may be observed in CPM patient, affecting the cerebellar peduncles, basal ganglia and the thalamus. Marchiafava Bignami disease is a rare hemispheric disconnection syndrome typically associated with chronic alcoholism. MBD often is associated with hypointense T1 weighted or hyperintense T2 weighted lesions of the corpus callosum, suggestive of demyelination. Alcohol discontinuation and nutritional supplementation may contribute to recovery from MBD.
Stimulant Dependence.
Cocaine dependence recently has been associated with an increased incidence of WMH on T2 weighted imaging studies an incidence rate for asymptomatic stroke of approximately 3% in abstinent former cocaine users. Abuse of amphetamine and methampetamine also have been associated with cerebral ischaemia.
Other Drugs
Lipophilic adulterants present in preparations of vaporized heroin may produce signs of a toxic leukoencephalopathy. Chronic use of combined heroin and cocaine has been associated with increased pituitary volume as well as reduced prefrontal and temporal cortex volume. Solvent abuse has been linked to loss of gray white matter tissue differentiation, increased perivascular white-matter signal hyperintensities and cerebral atrophy.
CONCLUSIONS:
While there are currently no clinical indications for ordering any of these fMRI techniques, they hold considerable promise for unraveling the neurocircuitry and metabolic pathways of psychiatric disorders in the immediate future and in further helping in psychiatric diagnosis and treatment planning.
REFERENCES:
1. Magnetic resonance imaging of Brain and spine, Third Edition, Volume – I, 2002, chapter 22, Page no = 1189-1205
2. Posse S, Muller-Gartner HW, Dager SR. Functional Magnetic Resonance Studies of Brain Activation. Seminars in Clinical neuropsychiatry 1996; 1:76-88.
3. Bonder JR, Swanson SJ, Hammeke TA Morris GL, Myeller WM, Fischer M, et al. Determination of language dominance using functional MRI: A comparison with the Wada test. Neurol 1996; 46:978-984.
4. Moseley ME, Decrespigny A, Spielman DM. Magnetic Resonance Imaging of Human Brain Function. Surgical neurology 1996; 45:385-391.
5. David A, Blamire A, Breiter H. Functional Magnetic Resonance Imaging: A new technique with implications for psychology and psychiatry. Brit J Psychiatry 1994: 164:2-7.
6. Menon RS, Ogawa S, Hu X, Strupp JP, Anderson P, Ugurbil K. BOLD based functional MRI at 4 Tesla includes a capillary bed contribution: echo-planar imaging correlates with previous optical imaging using intrinsic signals. Magn Res Med 1995; 33: 453-459
7. Belliveau JW, Kennedy DN, McKinstry RC, Buchbinder BR, weisskoff RM, Cohen MS, et al. Functional mapping of the visual cortex by MRI. Science 1991; 254: 716-719.
8. Harris GJ Lewis RF, Satlin A, English CD, Scott TM et al. Dynamic susceptibility contrast MRI of regional cerebral blood volume in Alzheimer’s disease. Am J psychiatry 1996; 153: 721-724
9. Fisher M, Prichard JW, Warach S. New magnetic resonance technique for acute ischaemic stroke, JAMA 1995; 274:908-911
10. Zivan JA. Diffusion-weighted MRI for diagnosis and treatment of ischaemic stroke. Ann neurol 1997;567-568
11. Moore CM, Renshaw PF. Magnetic Resonance Spectroscopy Studies of Affective Disorders. In: Krishnan KRR, Doraiswarmy PM, editors. Brain Imaging in Clinical Psychiatry. New York : marcel-Dekker, 1997:185-213
12. Frangou S, Williams SC. Magnetic resonance spectroscopy in psychiatry: Basic principles and applications. British Medical Bulletin 1996 ; 52:474-485
13. Pettigrew JW, withers G, panchalingam K, post JF. 31P nuclear magnetic resonance (NMR) spectroscopy of brain in aging and Alzheimer’s disease. J Neural Transm Suppl 1987; 24:261-268
14. Functional magnetic resonance imaging (fMRI) for the pshychiatrist Lorberbaum JP, Bohning DE, Shastri A, Nahas Z et al.
15. Dager SR, Strauss WL, Marro KI Richards TL, Metzger GD et al. Proton Magnetic resonance spectroscopy investigation of hyperventilation in subjects with panic disorder and Comparison subjects. Am J psychiatry 1995; 152:666-672
Sunday, July 29, 2007
MR MORPHOLOGY IN INTRACRANIAL TUBERCULOMAS
MR Morphology of Intracranial Tuberculomas
Dr. H. S. Das, Dr. N. Medhi, Dr. B. Saharia, Dr. S. K. Handique
Introduction:
Tuberculomas represent a common neurological disorder in developing countries, forming 12-30% of all intracranial masses – (1,2). Furthermore the incidence of intracranial TB in patients with AIDS is also increasing, the highest incidence recorded being 2.3% - (3,4) in one study to 18% in another – (5). Prompt diagnosis is mandatory since any delay in increased morbidity and mortality. Unfortunately the diagnosis is not always possible on the basis of clinical and epidemiological data, since clinical manifestations are nonspecific – (7,8) and objective evidence of systemic tuberculosis or exposure to the disease may be absent in upto 70% of the cases – (9). The role of CT in diagnosis of CNS tuberculomas in well established, nevertheless CT findings should be interpreted with caution since neoplastic, fungal or parasitic diseases may cause similar changes on CT – (10). Recently Magnetic Resonance (MR) Imaging has shown advantage over CT in the detection of intracranial pathology – (11) and its value in the diagnosis of infections diseases of the central nervous system (CNS) has been reported – (12,13). Although tubercular meningitis can not be differentiated from other meningitides on the basis of MR findings; but intraparenchymal tuberculomas show characteristic T2 shortening not found in most other space occupying lesions – (14). Thus in the appropiate clinical setting tuberculomas should be considered. Here, we report our experience in using MR for the evaluation of patients with intracranial tuberculoma.
Patients and Methods:
10 Patients with intracranial tuberculomas were evaluated with MR in our institution between August ’95 to August’ 99. 8 males and 2 females between 5-45 years (Mean 22.9 years) were included in this study. MRI was performed on a 1-tesla super conductive magnet. Standard spin echo techniques were used to obtain multiplanar T1 and T2 weighted images. Contrast was used in 6 patients. The diagnosis of CNS tuberculosis was made after proper integration of data from the surgical and medical findings. Data included positive biopsy in 2 patients; analysis of blood and CSF (elevation in 2 cases); positive response to anti tubercular drugs in 6 patients and MR findings. Initial CT was done upon admission to the hospital in all ten cases. MR was done to visualize the full extent of the lesion, to differentiate these lesions from other diseases affecting the brain and to delineate the contents (necrotic centre, capsule and surrounding edema). None of the patients tested positive for HIV.
Results:
Tuberculomas were supratentorial in 9 patients and infratentorial in 1. All but one patient had single lesions, which were located at the cortico-subcortical junction of the cerebral hemispheres and in the brainstem in 2 patients. 1 patient had a cerebellar tuberculoma. On MR intracranial tuberculoma caused prolongation of the T1 relaxation time which was most marked at the centre of the lesion. 5 patients had lesions hypointense to normal brain; 4 patients had lesions isointense and 1 patient had a mixed signal with hypointensity predominating on T1 weighted images. On the T2 weighted sequences the MR appearance varied. In six patients the centre of the lesion gave hypointense (dark) signal while the periphery gave a hyperintense (bright) signal relative to the brain parenchyma due to surrounding oedema. In 2 patients the centre of the lesion was hyperintense with a hypointense rim surrounded again by diffuse hyperintensity due to edema.
Follow up CT in 6 patients during the course of antituberculous drugs showed reduction in the six of the lesion as well as the oedema as a result of therapy. 2 patients positive biopsy while 2 patients were lost to follow up. Following contrast infusion in 6 patients ring enhancing lesions were observed in 4 patients, disc enhancing lesion size of less than 1 cm, 3 patients had lesion size of more then 2 cms while the lesion size varied between 1-2 cms in the rest of the 6 patients. 2 out of the 10 patients presented with meningitis, which shows diffuse thick meningeal contrast enhancement presumably due to granulation tissue. These 2 patients also had different degrees of hydrocephalus.
Discussion:
Tuberculomas develop in the brain when the initial Rich’s focus does not rupture into the meninges but expands locally within the parenchyma due to greater resistance of host tissues to the infecting organism (5). Meningitis can cause borderline encephalitis resulting in direct infiltration of the brain parenchyma and multiple small tuberculomas which coalesce to form mature tuberculomas – (16).
Tuberculomas have different appearances on T2 weighted images depending on their stage of evolution. At an early stage of formation of tuberculomas, an inflammatory reaction occurs; the mass has an abundance of giant cells and a capsule poor in collagen. At this stage the mass is isointense on T1 and T2 weighted images. At a later stage, the capsule becomes rich in collagen. When small tuberculomas coalesce to become larger lesions they give low signal on T2 weighted images because of fibrosis, scar tissue and free radicals produced by macrophages during active phagocytosis – (17).
22 of the 27 cases (84%) of NCS tuberculoma in the literature clearly showed low signal on T2 weighted images – (8, 18, 19, 20). 5 (16%) had lesions with central high signal thought to represent caseating pathologic examination revealed tuberculoma with dense reactive fibrosis.
In another study out of 97 patients presumed to harbour cerebral tuberculomas (of which 11 were confirmed by biopsy and 73 showed a therapeutic response to AKT) the lesions were either homogenously hypointense or revealed a central hyperintense nidus within the hypointense lesion on T2 weighted images (21).
Based on a histopathological grading of 7 proven tuberculomas, Gupta et al (22) concluded that the signal intensity on T2 weighted images is variable and dependant on the relative proportion of macrophages, cellular infiltrates and fibrosis. Granulomas, which were frankly hyperintense on T2 weighted images, exhibited increased cellular infiltrates, scantly macrophages and little fibrosis; while the hypointense lesions showed grater numbers of macrophages; more fibrosis and gliosis – (22). Large amounts of lipids were reported to contribute to the T2 shortening in 2 of the granulomas analysed by localized proton spectroscopy – (22). MR is of value to visualize the full extent of the lesion, in differentiation of the lesion with other diseases of the CNS (e.g. fungal granuloma, haemorrhagic metastases and “granulo-nodular” stage of neurocysticercosis) and to delineate the different components of the lesion (necrotic center, capsule and surrounding oedema), which is not always possible with CT.
References:
1. Dastur HM, Desai AD (1965): A comparitive study of brain tuberculomas and gliomas based upon 107 case records of each. Brain 88: 375-396.
2. Laitha VS, Marker FE, Dastur DK, tuberculosis of the Central Nervous System. Neurology (India) 1980; 28: 197-201.
3. Anderson KM, MacMillan JI (1975) Intercranial Tuberculoma: an Increasing Problem in Britain. I. Neurolo Neurosurg Pshchiatry 38: 194-201.
4. Bishburg E, Sundaram G, Reichan LB; Kapila R (1986) CNS tuberculosis with AIDS its related complexes. Ann Intern Med 105: 210-213.
5. Intracranial tuberculosis is AIDS: CT and MRI findings. M.F. villomoria, J Dela Torre, F. Fortea, L. Munoz, T. Hernadez and J. J. Alarcon: (1992) Neuroradiology 34: 11-14.
6. Harder E, Al-Jawi MZ; Carney P (1983): Intracranial Tuberculoma; Conservative management. Am J. Med 74: 570-576.
7. Lehrer H. Venkatesh B, Girolamo R, Smith A (1973): Tuberculoma of the brain (revisited) AJR 118 : 594-600.
8. Talamas O, Del Brutto OH; Garcia Ramos G (1989): Brainstem Tuberculoma; an analysis of 11 patients, Arch Neurol.
9. De Angelis LM (1981) Intracranial tuberculoma: Case report and review of literature. Neurology 31: 1133-1136.
10. Wrishber L, Nice C, Karx M (1984) Cerebral computer tomography : a text atlas, Saunders. Philadelphia.
11. Brant-Zawadzki M, Davis PL, Crooks LE (1983) : NMR demonstration of cerebral abnormalities : Comparision with CT AJNR 4 : 120-126.
12. Davidson HD, Steiner RE (1965) MRI in infections on the CNS AJNR 6 : 120-126.
13. Schorth G; Kretzchmar K; Gawehn J, Voigt K (1987): Advantages of MRI in the diagnosis of cerebral infection. Neuroradiology 29: 120-126.
14. Kioumehr, MR Dadsetan, SA Rooholamini, A, AU (1994): Central Nervous System Tuberculosis: MRI. Neuroradiology 36: 93-96.
15. Dastur DK, Lalitha VS: The many facets of neurotuberculosis. An epitome of neuropathology. In Zimmerman RA (ed). Progress in neuropathology Vol. 2 New York. Grune and Stration 1973, 351, 108.
16. Dastur DK, (1983) Neurosurgically relevant aspects and pathognesis of intracranial and intraspinal tuberculomas. Neurosurg Rev. 6 : 103-110.
17. Chang KH, Han MH, Roh JK et al (1990): Gd-DTPA enhanced MR Imaging in intracranial tuberculosis. Neuroradiology 32: 19-25.
18. Gupta RK, Jena A, Sharma A, Guha DK (1988) MR imaging of intracranial tuberculoma, J. computer Assist Tomong. 121: 280-285.
19. Salgado P, Del Brutto OH, Talamas O, Zenteno MA, Rodriguez Carbajal J, Neuroradiology (1989) 31 : 299-302. Intracranial tuberculoma: MR imaging.
20. Dastur HM (1983) Diagnosis and neurosurgical treatment in tuberculous diseases of the CNS. Neurosurgery 6: 11-113.
21. Desai SB, Shah VC, Tavri OJ, Rao P, MRI more specific than CT in cranial tuverculomas. Neuroradiology (1991) : 33 (Suppl).
22. Gupta RK, Pandey B, Khan EM, Mittal P, Gujral RB, Chhabra DK. Intra cranial tuberculomas: MRI signal intensity correlation with histopathology and localized proton spectroscopy. Mag. Res. Imaging (1993), 11: 443-449.
Dr. H. S. Das, Dr. N. Medhi, Dr. B. Saharia, Dr. S. K. Handique
Introduction:
Tuberculomas represent a common neurological disorder in developing countries, forming 12-30% of all intracranial masses – (1,2). Furthermore the incidence of intracranial TB in patients with AIDS is also increasing, the highest incidence recorded being 2.3% - (3,4) in one study to 18% in another – (5). Prompt diagnosis is mandatory since any delay in increased morbidity and mortality. Unfortunately the diagnosis is not always possible on the basis of clinical and epidemiological data, since clinical manifestations are nonspecific – (7,8) and objective evidence of systemic tuberculosis or exposure to the disease may be absent in upto 70% of the cases – (9). The role of CT in diagnosis of CNS tuberculomas in well established, nevertheless CT findings should be interpreted with caution since neoplastic, fungal or parasitic diseases may cause similar changes on CT – (10). Recently Magnetic Resonance (MR) Imaging has shown advantage over CT in the detection of intracranial pathology – (11) and its value in the diagnosis of infections diseases of the central nervous system (CNS) has been reported – (12,13). Although tubercular meningitis can not be differentiated from other meningitides on the basis of MR findings; but intraparenchymal tuberculomas show characteristic T2 shortening not found in most other space occupying lesions – (14). Thus in the appropiate clinical setting tuberculomas should be considered. Here, we report our experience in using MR for the evaluation of patients with intracranial tuberculoma.
Patients and Methods:
10 Patients with intracranial tuberculomas were evaluated with MR in our institution between August ’95 to August’ 99. 8 males and 2 females between 5-45 years (Mean 22.9 years) were included in this study. MRI was performed on a 1-tesla super conductive magnet. Standard spin echo techniques were used to obtain multiplanar T1 and T2 weighted images. Contrast was used in 6 patients. The diagnosis of CNS tuberculosis was made after proper integration of data from the surgical and medical findings. Data included positive biopsy in 2 patients; analysis of blood and CSF (elevation in 2 cases); positive response to anti tubercular drugs in 6 patients and MR findings. Initial CT was done upon admission to the hospital in all ten cases. MR was done to visualize the full extent of the lesion, to differentiate these lesions from other diseases affecting the brain and to delineate the contents (necrotic centre, capsule and surrounding edema). None of the patients tested positive for HIV.
Results:
Tuberculomas were supratentorial in 9 patients and infratentorial in 1. All but one patient had single lesions, which were located at the cortico-subcortical junction of the cerebral hemispheres and in the brainstem in 2 patients. 1 patient had a cerebellar tuberculoma. On MR intracranial tuberculoma caused prolongation of the T1 relaxation time which was most marked at the centre of the lesion. 5 patients had lesions hypointense to normal brain; 4 patients had lesions isointense and 1 patient had a mixed signal with hypointensity predominating on T1 weighted images. On the T2 weighted sequences the MR appearance varied. In six patients the centre of the lesion gave hypointense (dark) signal while the periphery gave a hyperintense (bright) signal relative to the brain parenchyma due to surrounding oedema. In 2 patients the centre of the lesion was hyperintense with a hypointense rim surrounded again by diffuse hyperintensity due to edema.
Follow up CT in 6 patients during the course of antituberculous drugs showed reduction in the six of the lesion as well as the oedema as a result of therapy. 2 patients positive biopsy while 2 patients were lost to follow up. Following contrast infusion in 6 patients ring enhancing lesions were observed in 4 patients, disc enhancing lesion size of less than 1 cm, 3 patients had lesion size of more then 2 cms while the lesion size varied between 1-2 cms in the rest of the 6 patients. 2 out of the 10 patients presented with meningitis, which shows diffuse thick meningeal contrast enhancement presumably due to granulation tissue. These 2 patients also had different degrees of hydrocephalus.
Discussion:
Tuberculomas develop in the brain when the initial Rich’s focus does not rupture into the meninges but expands locally within the parenchyma due to greater resistance of host tissues to the infecting organism (5). Meningitis can cause borderline encephalitis resulting in direct infiltration of the brain parenchyma and multiple small tuberculomas which coalesce to form mature tuberculomas – (16).
Tuberculomas have different appearances on T2 weighted images depending on their stage of evolution. At an early stage of formation of tuberculomas, an inflammatory reaction occurs; the mass has an abundance of giant cells and a capsule poor in collagen. At this stage the mass is isointense on T1 and T2 weighted images. At a later stage, the capsule becomes rich in collagen. When small tuberculomas coalesce to become larger lesions they give low signal on T2 weighted images because of fibrosis, scar tissue and free radicals produced by macrophages during active phagocytosis – (17).
22 of the 27 cases (84%) of NCS tuberculoma in the literature clearly showed low signal on T2 weighted images – (8, 18, 19, 20). 5 (16%) had lesions with central high signal thought to represent caseating pathologic examination revealed tuberculoma with dense reactive fibrosis.
In another study out of 97 patients presumed to harbour cerebral tuberculomas (of which 11 were confirmed by biopsy and 73 showed a therapeutic response to AKT) the lesions were either homogenously hypointense or revealed a central hyperintense nidus within the hypointense lesion on T2 weighted images (21).
Based on a histopathological grading of 7 proven tuberculomas, Gupta et al (22) concluded that the signal intensity on T2 weighted images is variable and dependant on the relative proportion of macrophages, cellular infiltrates and fibrosis. Granulomas, which were frankly hyperintense on T2 weighted images, exhibited increased cellular infiltrates, scantly macrophages and little fibrosis; while the hypointense lesions showed grater numbers of macrophages; more fibrosis and gliosis – (22). Large amounts of lipids were reported to contribute to the T2 shortening in 2 of the granulomas analysed by localized proton spectroscopy – (22). MR is of value to visualize the full extent of the lesion, in differentiation of the lesion with other diseases of the CNS (e.g. fungal granuloma, haemorrhagic metastases and “granulo-nodular” stage of neurocysticercosis) and to delineate the different components of the lesion (necrotic center, capsule and surrounding oedema), which is not always possible with CT.
References:
1. Dastur HM, Desai AD (1965): A comparitive study of brain tuberculomas and gliomas based upon 107 case records of each. Brain 88: 375-396.
2. Laitha VS, Marker FE, Dastur DK, tuberculosis of the Central Nervous System. Neurology (India) 1980; 28: 197-201.
3. Anderson KM, MacMillan JI (1975) Intercranial Tuberculoma: an Increasing Problem in Britain. I. Neurolo Neurosurg Pshchiatry 38: 194-201.
4. Bishburg E, Sundaram G, Reichan LB; Kapila R (1986) CNS tuberculosis with AIDS its related complexes. Ann Intern Med 105: 210-213.
5. Intracranial tuberculosis is AIDS: CT and MRI findings. M.F. villomoria, J Dela Torre, F. Fortea, L. Munoz, T. Hernadez and J. J. Alarcon: (1992) Neuroradiology 34: 11-14.
6. Harder E, Al-Jawi MZ; Carney P (1983): Intracranial Tuberculoma; Conservative management. Am J. Med 74: 570-576.
7. Lehrer H. Venkatesh B, Girolamo R, Smith A (1973): Tuberculoma of the brain (revisited) AJR 118 : 594-600.
8. Talamas O, Del Brutto OH; Garcia Ramos G (1989): Brainstem Tuberculoma; an analysis of 11 patients, Arch Neurol.
9. De Angelis LM (1981) Intracranial tuberculoma: Case report and review of literature. Neurology 31: 1133-1136.
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11. Brant-Zawadzki M, Davis PL, Crooks LE (1983) : NMR demonstration of cerebral abnormalities : Comparision with CT AJNR 4 : 120-126.
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Sunday, December 3, 2006
HEAD & NECK NODAL IMAGING
Cervical Nodes
Variable size. Typically, as many as 75 nodes are located on each side of the neck. Nodes contain a sub capsular sinus below a prominent capsule, into which lymphatic fluid drains. This capsule is often the first site of metastatic growth. The fluid permeates into the substance of the node (composed of a cortex and a medulla) and exits through the hilum to enter more lymphatic vessels. These nodes are located between the superficial cervical and prevertebral fascia and, thus, are very amenable to surgical removal. The lymphatic fluid eventually enters the venous system at the junction of the internal jugular and subclavian veins. Many nodal descriptions exist today; Rouvière's is the classic model.
The occipital nodes are in the superficial group, which includes 3-5 nodes. This group of nodes is localized between the sternocleidomastoid (SCM) and trapezius muscles, at the apex of the posterior triangle. These nodes are superficial to the splenius capitis. The deep group includes 1-3 nodes. This group of nodes is located deep to the splenius capitis and follows the course of the occipital artery. These nodes drain the scalp, the posterior portion of the neck, and the deep muscular layers of the neck.
The postauricular nodes vary in number from 2 to 4; they are located in the fibrous portion of the superior attachment of the SCM muscle to the mastoid process. Postauricular nodes drain the posterior parietal scalp and the skin of the mastoid region.
The parotid nodes can be divided into intraglandular and extraglandular groups. The extraglandular parotid nodes are located outside but adjacent to the parotid gland, where they drain the frontolateral scalp and face, the anterior aspects of the auricle, the external auditory canal, and the buccal mucosa. Embryologically, the lymphatic system develops before the parotid gland, which surrounds the intraglandular nodes as it develops. The intraglandular nodes drain the same regions as the extraglandularnodes, to which they interconnect and then drain into the upper jugular group of lymph nodes. As many as 20 parotid nodes may be found.
The submandibular nodes are divided into 5 groups:
Preglandular, postglandular, prevascular, postvascular, and intracapsular. The preglandular and prevascular groups are located anterior to the submandibular gland and facial artery, respectively. The postglandular and postvascular groups are posterior to these structures. Differing from the parotid gland in embryological development, there is no true intraglandular node; however, occasionally, a node has been identified inside the capsule of the gland. The submandibular nodes drain the ipsilateral upper and lower lip, cheek, nose, nasal mucosa, medial
canthus, anterior gingiva, anterior tonsillar pillar, soft palate, anterior two thirds of the tongue, and submandibular gland. The efferent vessels drain into the internal jugular nodes. For the submental nodes, 2-8 nodes are located in the soft tissues of the submental triangle between the platysma and mylohyoid muscles. These nodes drain the mentum, the middle portion of the lower lip, the anterior gingiva, and the anterior third of the tongue. The efferent vessels draininto both the ipsilateral and contralateral submandibular nodes or into the internal jugular group.
The sublingual nodes are located along the collecting trunk of the tongue and sublingual gland and drain the anterior floor of the mouth and ventral surface of the tongue. These nodes subsequently drain into the submandibular or jugular group of nodes.
The retropharyngeal nodes are divided into a medial and lateral group, located between the pharynx and the prevertebral fascia. The lateral group, located at the level of the atlas near the internal carotid artery, consists of 1-3 nodes, which may extend to the skull base. The medial group extends inferiorly to the postcricoid level. This group drains the posterior region of the nasal cavity, sphenoid and ethmoid sinuses, hard and soft palates, Nasopharynx, and posterior pharynx down to the postcricoid area. Management of these nodes must be considered if any Malignancy arises from the mentioned drainage areas.
The anterior cervical nodes are divided into the anterior jugular chain and the juxtavisceral chain of nodes. The anterior jugular chain nodes follow the anterior jugular vein, located superficial to the strap muscles. These nodes drain the skin and muscles of the anterior portion of the neck, and the efferent vessels empty into the lower internal jugular nodes. The juxtavisceral nodes are separated into the prelaryngeal, parathyroid, pretracheal, and paratracheal nodes. Prelaryngeal nodes are located from the thyrohyoid membrane to the cricothyroid membrane and drain the larynx and the thyroid lobes. A single Delphian node is often found overlying the thyroid cartilage.
The pretracheal group consists of nodes between the isthmus of the thyroid gland down to the level of the innominate vein. Varying from 2-12 in number, these nodes drain the region of the thyroid gland and the trachea and receive afferent flow from the prelaryngeal group. The pretracheal efferents empty in the internal jugular group and the anterior superior mediastinal nodes.
The paratracheal nodes lie near the recurrent laryngeal nerve and drain the thyroid lobes, parathyroid glands, subglottic larynx, trachea, and upper esophagus. The efferent vessels travel to the lower jugular group or directly toward the junction of the internal jugular vein and theSubclavian vein. The anterior nodes drain bilaterally because the midline of the neck has no division. Treatment must be planned accordingly when a tumor is located in subjacent draining areas.
The lateral cervical nodes are divided into superficial and deep groups. The superficial group follows the external jugular vein and drains into either the internal jugular or transverse cervical nodes of the deep group. The deep group forms a triangle bordered by the internal jugular nodes,the spinal accessory nodes, and the transverse cervical nodes. The transverse cervical nodes, forming the base of the triangle, follow the transverse cervical vessels and may contain as many as 12 nodes. These nodes receive drainage from the spinal accessory group and from collecting trunks of the skin of the neck and upper chest. The spinal accessory chain follows the nerve of the same name and may account for as many as 20 nodes. This chain receives lymph from the occipital, postauricular, and suprascapular nodes and from the posterior aspect of the scalp, nape of the neck, lateral aspect of the neck, and the shoulder.
The internal jugular chain consists of a large system covering the anterior and lateral aspects of the internal jugular vein, extending broadly from the digastric muscle superiorly to the subclavian vein inferiorly. As many as 30 of these nodes may exist, and they have beenarbitrarily divided into upper, middle, and lower groups. The efferents of these nodes eventually pass into the venous system via the thoracic duct on the left and multiple lymphatic channels on the right. These nodes drain all the other groups mentioned. Direct efferents may be present from the nasal fossa, pharynx, tonsils, external and middle ear, Eustachian tube, tongue, palate, laryngopharynx, major salivary glands, thyroid, and parathyroid glands. Although fairly consistent, these drainage patterns are subject to alteration with malignant involvement or after radiotherapy. In such cases, rerouting is possible, with metastases arising in unusual sites.Metastases have also been shown to skip first-echelon nodes and manifest in the lower internal jugular group.
The most widely accepted terminology was originally described by a group of head and necksurgeons at Memorial Sloan-Kettering Hospital. This classification uses neck levels or zones and divides each side of the neck into 6 separate regions. Level I is bordered by the body of the mandible, anterior belly of the contralateral digastric muscle, and anterior and posterior bellies of the ipsilateral digastric muscle. Two nodal subgroups are found. The submental group (Ia) is found in the submental triangle (anterior belly of the digastric muscles and the hyoid bone), and the submandibular group (Ib) is found within the submandibular triangle (anterior and posterior bellies of the digastric muscle and the body of the mandible).
The nodes found in level II are located around the upper third of the internal jugular vein, extending from the level of the carotid bifurcation inferiorly to the skull base superiorly. The lateral boundary is formed by the posterior border of the SCM muscle; the medialboundary is formed by the stylohyoid muscle. Two subzones are also described; nodes located anterior to the spinal accessory nerve are part of level IIa, and those nodes posterior to the nerve are located in level IIb. The middle jugular lymph node group defines level III. Nodes are limited by the carotid bifurcation superiorly and the cricothyroid membrane inferiorly. The lateral border is formed by the posterior border of the SCM muscle; the medial margin is formed by the lateral border of the sternohyoid muscle. Level lV contains the lower jugular group and extends superiorly from the omohyoid muscle to the clavicle inferiorly. The lateral border is formed by the posterior border of the SCM muscle; the medial margin is formed by the lateral border of the sternohyoid muscle. The lymph nodes found in level V are contained in the posterior neck triangle, bordered anteriorly by the posterior border of the SCM muscle, posteriorly by the anterior border of the trapezius, and inferiorly by the clavicle. Level V includes the spinal accessory, transverse cervical, and supraclavicular nodal groups. Level VI lymph nodes are located in the anterior compartment. These nodes surround the middle visceral structures of the neck from the level of the hyoid superiorly to the suprasternal notch inferiorly.
Evaluating neck metastases based on physical examination findings has been the classic method for patients with new tumors in the head and neck. The single most important factor in determining prognosis is whether nodal metastasis is present. Survival rates decrease by 50% when nodal metastases are present. Furthermore, the presence of cervical adenopathy has been correlated with an increase in the rate of distant metastasis. During the clinical evaluation, carefully palpate the neck, with specific attention to location, size, firmness, and mobility of each node. Direct attention to nodes that appear fixed to underlying neurovascular structures or visceral organs or that demonstrate skin infiltration. The description of each node becomes an important part of the medical record, which can be used to assess the response to treatment or the progression of the disease.
Unfortunately, clinical palpation of the neck demonstrates a large variation of findings among various examiners. Although both inexpensive to perform and repeat, palpation findings are generally accepted as inaccurate. Both the sensitivity and specificity are in the range of 60-70%, depending on the tumor studied. Because of the known low sensitivity and specificity of palpation, a neck side without palpable metastases is at risk of harboring occult metastasis, with the risk determined by the characteristics of the primary tumor. The incidence of false-negative (occult) nodes based on physical examination findings varies in the literature from 16-60%. Before the introduction of diagnostic imaging, particularly CT scan, clinical palpation was shown to be inadequate for detecting cervical metastasis. Soko et al reported that only 28% of occult cervical metastases were found by clinical palpation. Martis reported a 38% prevalence of occult metastasis based on clinical examination findings
Debate persists over the relative merits of imaging in the evaluation of the neck for metastatic disease. Studies that correlate radiologic and histopathologic findings show that early microscopic metastases can be present in nodes smaller than 10 mm that demonstrate no stigmata of neoplasia (i.e., central necrosis, extracapsular spread). Evidence of early metastatic disease in clinically occult nodes is minimal and may evade the efforts of the pathologist and radiologist.
Ultrasound :
Ultrasound is reported superior to clinical palpation for detecting lymph nodes and metastases. The advantages of ultrasound over other imaging modalities are price, low patient burden, and possibilities for follow-up.
Sonographs of metastatic lymph node disease characteristically find enlargement with a spherical shape. Commonly, nodes are hypo echoic, with a loss of hilar definition. In cases of extranodal spread with infiltrative growth, the borders are poorly defined. Common findings of metastases from squamous cell carcinoma are extranodal spread and central necrosis together with liquid areas in the lymph nodes. Lymph node metastases from malignant melanoma and papillary thyroid carcinoma have a nonechoic appearance that mimics a cystic lesion. Sonography also is useful for assessing invasion of the carotid artery and jugular vein. Because lymph nodes of borderline size cannot be reliably diagnosed using ultrasound alone, ultrasound-guided fine-needle aspiration and cytologic examination of the nodes in question can be easily performed. The result of the aspirate examination depends on the skill of the ultrasonographer and the quality of the specimen (ie, harboring an adequate number of representative cells). Using this technique, most studies report that a sensitivity of up to 70% can be obtained for the N0 neck.
CT scans
Since its debut in the 1970s, CT scans have been an invaluable tool in all fields of medicine, including the evaluation of head and neck cancer. Since the advent of high-resolution systems and specific contrast media, fine-cut CT scanning has allowed the detection of pathological cervical nodes of smaller size that may be missed by clinical examination. CT scanning is now used routinely for the preoperative evaluation of the neck because, presumably, it helps decrease the incidence of occult cervical Lymphadenopathy. Introduced in 1998, multiple-spiral CT scanning promises further improvement of temporal and spatial resolution (in the longitudinal axis). This technique permits rapid scanning of large volumes of tissue during quiet breathing. The volumetric helical data permit optical multiplanar and 3-dimensional reconstructions. Improvement of the assessment of tumor spread and lymph node metastases in arbitrary oblique planes is another advantage of the spiral technique.
Criteria for the identification of questionable nodes are also evolving as technology advances. Central necrosis remains the most specific finding suggestive of nodal involvement, but its absence does not exclude metastasis. Unfortunately, metastasis is usually quite rare or not visible in small lymph nodes, where detection would be crucial. Because of the higher imaging resolution, various studies have reduced the traditional values of 10-15 mm for a node to be suggestive. Many authors have proposed a minimal axial diameter of 11 mm for the submandibular triangle and 10 mm for the rest of the neck. Other criteria include the presence of groups of 3 or more borderline nodes and the loss of tissue planes.
Magnetic resonance imaging
The value of MRI is its excellent soft tissue resolution. MRI has surpassed CT scanning as the preferred study in the evaluation of cancer at primary sites such as the base of the tongue and the salivary glands. The sensitivity of MRI exceeds that of clinical palpation in detecting occult cervical lymphadenopathy. Size, the presence of multiple nodes, and necrosis are criteria shared by CT scanning and MRI imaging protocols. Most reports indicate that CT scanning still has an edge over MRI for detecting cervical nodal involvement. Advances in MRI technology (eg, fast spin-echo imaging, fat suppression) have not yet surpassed the capacity of CT scanning to identify lymph nodes and to define nodal architecture. Central necrosis, as evaluated by unenhanced T1- and T2-weighted images, has been shown to provide an overall accuracy rate of 86-87% compared with CT scanning, which has an accuracy rate of 91-96%. The use of newerContrast media, especially supramagnetic contrast media agents, hopefully will improve the sensitivity of MRI.
Positron emission tomography and single-photon emission computed tomography
Some studies have demonstrated that positron emission tomography may be able to detect nodal metastases in lymph nodes that are negative for disease based on CT scan or MRI findings. Single-photon emission computed tomography imaging with fluorodeoxyglucose or thallium also reportedly detects nodal metastases. The use of positron emission tomography in combination with immunoimaging using monoclonal antibodies might further enhance accuracy.
None of the currently available imaging techniques can help depict small tumor deposits inside lymph nodes. Characteristics of metastatic lymph nodes that can be depicted are the size and presence of noncontrast-enhancing parts inside metastatic lymph nodes caused by tumor necrosis, tumor keratinization, or cystic areas inside the tumor. Only rarely does tumoral tissue enhance more than reactive lymph node tissue; in these rare cases, the tumor can be visualized within a reactive lymph node.
Patients who need an evaluation for a possible nodal malignancy require a comprehensive multidisciplinary evaluation of all potential sites of drainage to that node to identify its primary source. This includes a thorough evaluation of potential primary sites using endoscopic techniques. When appropriate, include laryngoscopy, esophagoscopy, bronchoscopy, and examination of the nasopharynx. If no primary source is identified, taking blind mucosal biopsy samples of the most likely head and neck subsites is essential. Complete documentation of nodal characteristics by clinical examination and palpation guide the examiner in using adjunctive radiological tools to exclude occult nodal metastasis
References:
Chen Z, Malhotra PS, Thomas GR, et al: Expression of proinflammatory and proangiogenic cytokines in patients with head and neck cancer. Clin Cancer Res 1999 Jun; 5(6): 1369-79[Medline].
Curtin HD, Ishwaran H, Mancuso AA, et al: Comparison of CT and MR imaging in staging of neck metastases. Radiology 1998 Apr; 207(1): 123-30[Medline].
Haor SP, Ng SH: Magnetic resonance imaging versus clinical palpation in evaluating cervical metastasis from head and neck cancer. Otolaryngol Head Neck Surg 2000 Sep; 123(3): 324-7[Medline].
Merritt RM, Williams MF, James TH, Porubsky ES: Detection of cervical metastasis. A meta-analysis comparing computed tomography with physical examination. Arch Otolaryngol Head Neck Surg 1997 Feb; 123(2): 9-52[Medline].
Safa AA, Tran LM, Rege S, et al: The role of positron emission tomography in occult primary head and neck cancers. Cancer J Sci Am 1999 Jul-Aug; 5(4): 214-8[Medline].
Southwick, HW, Slaughter, DP, Trevino, ET: Elective neck dissection for intraoral cancer. Arch Surg 1960; 80: 905-9.
Stacker SA, Caesar C, Baldwin ME, et al: VEGF-D promotes the metastatic spread of tumor cells via the lymphatics. Nat Med 2001 Feb; 7(2): 186-91[Medline].
Van den Brekel MW: Lymph node metastases: CT and MRI. Eur J Radiol 2000 Mar; 33(3): 230-8[Medline].
Thursday, September 29, 2005
MAGING IN CEREBRAL VASCULAR PATHOLOGIES: EVOLUTION OF INTRACRANIAL HEMATOMA
IMAGING IN CEREBRAL VASCULAR PATHOLOGIES:
EVOLUTION OF INTRACRANIAL HEMATOMA
1. Immediate
- liquid with 95% O2 saturated Hb, T2 hyper, T1 iso within seconds platelets thrombi form & cells aggregate
2. Hyper acute stage -
4-6 hrs, fluid serum begins to disperse
Protein clot retracts, red cells become spherical,
Early peripheral edema begins, T2 iso, T1 iso
OxyHb is diamagnetic with no unpaired electrons,
CT - isodense for 1-3hrs, then becomes dense, 60-100HU
3. Acute stage
- 7-72 hrs, red cells begin to compact, deoxyhb
Central portion T2 hypo, T1 iso
DeoxyHb is paramagnetic with 4 unpaired electrons, T2 shortening
Sheilded from H2O by globin, prevents T1 shortening
No proton-electron relaxation enhancement can occur
Edema pronounced in periphery
Dense on CT, window width of 150-250 best
4. Subacute stage -
1-4 wks, methemoglobin starts day 4
Begins at periphery & progresses towards anoxic center
Cells begin to lyse at 1 week releasing metHb, decrease in edema
Perivascular inflammatory reaction begins with macrophage at periphery
Ring Enhancement caused by this process
T1 BRIGHT due to 5 unpaired electrons exposed by globin change
Proton-electron relaxation enhancement does occur
Periphery affected 1st, middle remains iso initially
T2 HYPO early when methemoglobin still in RBC
BRIGHT once the cell breaks down & Hb diluted in water
CT attenuation decreases approx 1.5HU per day
CT is NOT an accurate indicator of age, due to variable Hb etc
5. Early Chronic stage
- >4wks, edema & inflammatory reaction subside
Vascular proliferation encroaches on haematoma decreasing its size
Dilute uniform pool of extracellular metHb with vascular walls
Macrophage contain ferritin & hemosiderin at periphery
T2 hypo due to strong magnetic susceptibility
T1 iso due to fact that hemosiderin is water insoluble
Hypodense on CT unless rebleeding has occurred
6. Late Chronic stage -
cystic or collapsed with dense capsule
Vascular proliferation gradually forms fibrotic matrix with macrophage
Infants may resolve completely
Ferritin laden scar persists for years in adults
10% calc with residual hypodense focus in 40%
Gradient echo is helpful in detecting Haem in low field MRI's
OVERVIEW OF HEMORRHAGE CAUSES
Underlying cause often hidden by the bleed. Intraventricular extension associated with 10% mortality
1. Neonatal Hemorrhage - germinal matrix hemorrhage secondary to prematurity
thin walled, proliferating vessels in subependyma of lateral caudothalamic groove
involution occurs at 34 wks when all cells have migrated
No hemorrhage in utero or beyond first 28 days post birth
Grade I - Hemorrhage confined to germinal matrix, can be bilateral
Grade II - rupture into normal size ventricles
Grade III - intraventricular hemorrhage with Hydrocephalus
Grade IV - extension to adjacent hemispheric white matter
Can be seen by US in acute & subacute, lucent if chronic
Term Infants - Hemorrhage usually secondary to trauma, subdural mostly
Asphyxia & infarction most commonly in non-traumatic cases
Posterolateral lentiform nuclei & ventral thalamus most susceptible
2. Hypertension – Most common cause of nontraumatic bleed in adult
Lenticulostriate & Pontine vasculatures mostly involved, penetrating branches of MCA
Usually spontaneous in elderly patients, basal ganglia mostly
Vessels often abnormal, ruptured microanuerysms etc
50% have hemorrhage dissection into ventricles, poor prognosis
Lobar white matter hemorrhage in 20%, cerebellum 10%, midbrain & brainstem rare
Originates along perforating branches near dentate nuclei
Active bleeding usually lasts <1hr
Edema progresses for 24-48hrs, 25% die in this period
Hypertensive Encephalopathy - occurs secondary to elevated BP
Toxemia (Most common) - autoregulation overwhelmed especially in posterior aspect
Overdistention of arteriole leads to BBB breakdown
Reversible vasogenic edema results, frank hemorrhage rare
Cortical petechia & subcortical hemorrhage possible, especially in occipital regions
Increased T2 in external capsule & basal ganglia more common
Chronic renal Diseases, TTP, & Hemolytic-Uremic syndrome other causes
3. Hemorrhagic Infarction
Arterial Infarction - hemorrhage when endothelium reperfused
Occurs in 50%, but only seen in 10%, sensitivity: MRI>CT
Cortex & basal ganglia from MCA distribution most commonly, 24-48hrs later
Pseudolaminar Cortical Necrosis - generalized hypoxia
Middle layers usually effected, gyriform hemorrhage
Nonhemorrhagic ischemic changes can occur, gyri calcification possible
Venous Infarction - usually associated with dural sinus thrombosis
Dura around sinus will enhance, clot stays hypodense (empty delta sign)
More likely to effect white matter than cortex
4. Aneurysms - 90% of nontraumatic subarachnoid hemorrhage
Headache common presenting sign for aneurysm, CT best for acute SAH
Blood usually fills ambient cisterns & sylvian first
90% of blood cleared from CSF in 1wk
MRI better for subacute or chronic SAH, dirty CSF
Superficial siderosis - hemosiderin deposit on meninges
Cerebellum brainstem & cranial nerves also coated - neurological dysfunction
Giant aneurysms >2.5cm often have intramural hemorrhage
most from carotid, cavernous portion most common, all ages
75% have calc if thrombosed, none otherwise
Charcot-Bushard Aneurysm - secondary to HTN
5. Vascular Malformations -
AVM & Cavernous Angioma commonly
Most bleed into parenchyma rather than subarachnoid space
Arteriovenous Malformation - pial, dural or mixed, No cap bed
Pial AVM's - hemorrhage @ 2% per year, often in previously normal young pts
70% bleed by 1st exam, repeated hemorrhage can simulate neoplasm
Central nidus with gliosis & encephalomalacia
Dural AVM's - no central nidus, SAH or subdural
hemorrhage rare unless drainage through cortical veins
Cavernous Angioma - bleed @ .5% per year, freq repeated bleeds
Popcorn like with mixed signal foci & hemosiderin ring
Venous Angiomas - bleed rare, similar hematoma of other malformations
Medusa like collection of dilated medullary veins
Capillary Telangiectasias - usually small & clinically silent
may see multiple small foci of hemosiderin on T2
INTRACRANIAL ANEURYSMS & VASCULAR MALFORMATIONS
Charcot-Bushard Aneurysm - secondary to Hypertension
20% multiple, higher incidence in females.
Look for familial causes such as Polycystic Kid Disease
SACCULAR ANEURYSMS
Berrylike out pouching from arterial bifurcation
Include intima & adventitia, media ends with normal vessel
1. Etiology - hemodynamic induced injury, abnormal shear forces most commonly
Trauma, infection, tumor, drug abuse & AV malformations
Berry Aneurysms - associated with polycystic kidney Diseases & aortic coarctation
2. Incidence - 1% of angios & 5% of postmortems
Multiple in 20%, esp in females & polycystic kidney Diseases
Bilateral in 20%, esp at cavernous sinus, Pcom & MCA trifurcation
Occur age 40-60 unless traumatic or mycotic,
3. Associated Conditions - occur at anomalous vessels & AVM
Inc pressure ie HTN & aortic coarctation
Systemic Diseases - Marfan’s, fibromuscular dysplasia, polycystic kidney diaeases
4. Location - 30% at anterior communicating, 30% at posterior communicating, 20% MCA origin
10% in post circulation especially basilar artery bifurcation
traumatic or mycotic occur anywhere
5. Clinical Presentation - asymptomatic until rupture or giant >2.5cm
1-2% risk of rupture per year, 3.5% risk of surg
No different risk with HTN, age, sex or multiplicity
All should be repaired if >3yr life expectancy
Subarachnoid Hem - clinical grade by Hunt & Hess scale I-V
Vasospasm most common cause of morbidity, 30% die
highest bleed rate in 1st 24hrs, 50% rebleed in 2wk
CT - shows SAH in >80% of ruptured aneurysms
Cavernous sinus aneurysms can compress Nerves III-VI
TIA, Seizures & embolic ischaemia less common
Giant Aneurysms - most from supraclinoid carotid, all ages
Fibrous vascular walls, rarely rupture, Symptoms secondary to mass effect
Partially Thrombosed Aneurysms - 75% have curvilinear calcification
CT most specific for these with target seen
NO calc if not thrombosed
D/D - Meningioma, both erode sella & lat sphenoid
aneurysm has no associated hyperostosis or atherosclerosis
6. Appearance of Saccular Type - catheter angiography definitive
asses for relation to vessel, adjacent branches & vasospasm
essential in assessment of nontraumatic SAH
Thrombosed aneurysm will have no finding, 15%
may see mass effect if large
irregularity or local vasospasm can indicate rupture
D/D vascular loops & infundibuli (embryonic funnel <2mm)
CT may show bone erosion in long standing case
Patent aneurysms enhance intensely w contrast
Location of SAH can be prognostic indicator
Ambient cisterns anterior to brainstem probably just venous rupture
No repeat angio needed
Suprasellar cistern to lateral sylvian fissure
more aneurysmal pattern, must do F/U angio
MRI dependent on pattern of flow, turbulence & clot
may have wall enhancement with gadodiamide, laminated with thrombosis
7. Traumatic Aneurysm - <1%,>
nonpenetrating usually occur at skull base, or shear
hyperextention stretches ICA over lat C1
8. Mycotic Aneurysms - Secondary to infection of arterial wall, rare <10%
adventitia & muscularis disrupted, thoracic aorta commonly
Angio - occur dist to usual location, 2nd branch MCA commonly
most common cause of multiple MCA aneurysms
usually small, staph & strep most common, inc in child
bleed into parenchyma or SAH equal incidence
Medical Treatment usually sufficient to control, surgery if enlarge on angio
Mucor & Aspergilla invade direct from nasopharynx cause thrombosis & infarct more often than aneurysm
9. Oncotic Aneurysms - usually extra cranial, exsanguinate freq
tumor may implant or cause emboli, primary or metastatic
10. Flow-Related Aneurysms - seen with AVM's in 30%
distal ones most likely to hemorrhage
11. Vasculopathies - rare but seen with SLE, infarct & TIA commonly
Takayasu's Arteritis - 9:1 female, inflammation & stenosis most commonly
prox arch vessels, L subclavian commonly, often occludes
Fibromuscular Dysplasia - up to 50%, dissection & A-V fistula, 65% bilateral
Cocaine - 50% with CNS symptoms have SAH, may be secondary to HTN treatment
several drugs cause vasculitis .
FUSIFORM ANUERYSMS
Etiology - atherosclerosis, exaggerated arterial ectasia
media damaged, stretches & elongates, frequent mural thrombus
Vertebrobasilar Dolichoectasia - Common site, older patient
often thrombus producing brainstem infarcts
can also compress local stem causing nerve palsies
Imaging - enhances if patent, hyperintense if thrombosed
curvilinear calcification pathognomonic, may cause skull base erosion
DISSECTING ANEURYSMS
Etiology - intramural blood from tear in intima
may narrow or occlude lumen, may distend subadventitia
do not confuse with Pseudoaneurysm, a encapsulated hematoma
Presentation - usually extracranial unless severe trauma
Commonly in midcervical ICA & vertebral from C2 to skull base
Catheter angio remains procedure of choice for assesment
INTRACRANIAL VASCULAR MALFORMATIONS
1. Parenchymal AVM - congenital, dilated arteries & veins without capillary bed
98% solitary, multiple in Osler-Weber-Rendu & Wyburn-Mason
Incidence - 85% supratentorial, peak 20-40y, 25% children
Hemorrhage in 85% with 3% per year risk, seizure 25%, deficit 25%
Size not predictive, deeper & smaller ones bleed more
Parenchymal commonly, also common cause of SAH if <20yrs,>
Vascular Steal - atrophy due to vasculopathy of feeding vessel
atrophic low density regions & hematoma with high density
Overlying meninges thick & hemosiderin stained
Angio - shows feeding arteries & tortuous veins
often wedge shaped, possible to appear Normal if thrombosed
GBM may simulate but usually has tissue between vessels
10% have aneurysms in feeding arteries, can bleed
Cryptic AVM's - not seen by angio, 10%
CT - often absent w/o contrast, 25% have mild curvilinear calcification
mixed increased & decreased density if seen, Mild mass effect possible
Enlarged post venous sinuses but not cavernous sinus
Calcification seen in <1/3,>
MRI - honeycomb of flow voids, increased signal if thrombosed
hemorrhage in different stages often present
No significant intervening brain tissue, D/D : GBM
TX - resection if unruptured, must be completely removed
Aneurysms must be treated separately, increased risk for bleed
2. Dural AVM's & Fistulae - form within a venous sinus
no discrete nidus, multiple microfistulae, occluding sinus frequent
Follow recanulation of thrombosed sinus, 10% of all AVM's
Transverse or Sigmoid sinus commonly, Bruits & headache most common
Cavernous sinus AVM - proptosis, retro orbital pain, proptosis
SAH common if reflux flow forced into cortical veins
Carotid-Cavernous fistula related, follow trauma
Occipital & Meningeal branch of ext carotid #1 feeders
CT often N, MRI may show dilated cortical veins
3. Mixed - 15%, if parenchymal AVM recruits arteries from dural supply
4. Capillary Telangiectasias - multiple nests of dilated capillaries
Common in pons & Cerebellum, usually incidental
Gliosis of adjacent brain & hemosiderin staining from hem possibly
Cavernous Angiomas assoc or simply the extreme form
Osler-Weber-Rendu - hereditary hemorrhagic Telangiectasias
25% have brain abnormalities, most are true AVM's
Visceral angio dysplasia with scalp & mucous membrane telangiectasia
2nd most common lesion to venous angioma at autopsy
Not visualized by angio, may present with epistaxis
CT may faintly enhance, faint on MRI
5. Cavernous Angiomas - Hemangioma or cavernoma
Circumscribed nodule of honeycomb sinusoidal vascular spaces
separated by fibrous bands but no intervening neural tissue
frequently MULTIPLE HEMATOMAS at different stages, reticulated core of vessels
Supratentorial 80% but can occur anywhere, 50% multiple
Most Common vascular lesion identified, 20-40y/o
Seizure, deficits & bleed most common presenting features
Angio does NOT visualize, possible faint blush in early venous
CT shows freq Calc, variable enhancement, can simulate neoplasm
MRI - popcorn like appearance on T2 due to multiple hem
multiple areas of signal drop-out due to hemosiderin
VENOUS MALFORMATIONS
1. Venous Angioma - dilated anomalous veins converge on central vein
Etiology - remnant embryonic venous system, usually solitary
assoc with migrational abnormalities & cavernous Angiomas in 30%
Asymptomatic, Hemorrhage very rare unless from associated cavernous angioma
CT - may show linear tuft of vessels post contrast
located in deep White Matter of cortex or Cerebellum, commonly adjacent to frontal horn
MRI - shows stellate tributary veins into prominent collector vein
gliosis or hemorrhage seen in only 15%
Angio - the only vascular malformation with a single draining vein
Medusa head appearance on venous phase of angio
2. Vein of Galen Aneurysm - enlargement of Galenic system
Secondary to arteriovenous fistulae from choroidal arteries
AVM in thalmus or midbrain can also cause this
Present at birth with high-out put cardiac failure, cranial bruit +
Macrocephaly with obstructive hydrocephalus, deficits & ocular symptoms
US shows bi-directional flow in vein of Galen
Angio demonstrates either choroidal artery or thalmoperforating feeder
dilation to venous varix with or without distal stenosis
if stenosed distally will often thrombose
CT - large enhancing midline mass posterior to 3rd ventricle
Hydrocephalus frequent but hemorrhage rare
enhancing serpentine vessels in thalamic region
3. Venous varix - assoc with several intracranial vascular abnormalities
Enlarged & thin veins resulting in SAH, hydrocephalus & increased ICP
Sinus Pericranii - venous haemangioma adherent to outer skull, deep to galea
supplied from intracranial sinus & blood returns to sinus
present with enlarging fluctuant soft tissue mass, enlarge with crying
often secondary to trauma, often resolved with prolonged compression
Frontal commonly, parietal next, most near sagittal sinus, can be very lateral
Skull Film - usually sharp margins, vascular honeycombs possible
CT - shows strong uniform enhancement
MRI - well delineated ovoid or fusiform areas w variable signal
Venous Cavernoma - subcutaneous lesions of scalp
blood supply from external carotid, drain to external jugular
4. Orbital Venous Varix - rare vascular malformation in orbit
Causes intermittent proptosis & diplopia with valsalva & bending over
Disappear completely with axial views, use tourniquet on jugular vein
NEONATAL HEMORRAGE
Caudothalamic groove - between head of caudate & thalamus
both make up lateral wall of lateral ventricle, terminates in Monroe
Foramen of Monroe - divides frontal & body portions of ventricles
thalmus entirely posterior, caudate head anterior, choroid enters it
1. Subependymal Hemorrhage - preterm infants <32wks
Correlates with size of germinal matrix at birth, largest 24-32wks
involutes & is absent by 40wks, last in inferior lateral wall of frontal
lies inferior to ependyma, superior to head of caudate & anterior to thalmus
Usually occurs in first 3 days, always by 7-8 days
Grade 0 – Normal
Grade I - Subependymal alone
Grade II - intraventricular with no ventriculomegaly
Grade III - Hydrocephalus,
Grade IV - intraparenchymal
grade does not predict ultimate outcome, may progress
Serial studies required, only applies to germinal matrix hemorrhage
2. Parenchymal Hemorrhage - extends farther lateral than germinal matrix
can be "grade IV", but not all secondary to germinal matrix bleed
most extend from SHE(Subependymal haemorrhage) to frontal or parietal lobes
Hypoxia & Hypercapnia implicated as etiology
stress causes vessels to dilate & burst
Phase 1 - echogenic like SEH for 1-2wks
Phase 2 - central Hypoechoic, bright peripheral rim 2-4wks
Phase 3 - retracts & settles into dependent position
Phase 4 - necrosis & phagocytosis complete, encephalomalacia
Cerebellar hematoma best scaned in coronal behind ear
assoc with mortality of 50%.
3. Choroidal Hemorrhage - usually grade II or III
Second cause of intraventricular hemorrhage not caused by SEH
Difficult to discern from normal choroid on US
asym scanning can show marked asym in choroid size
isolated choroid hematoma simulates ventricular hematoma with no hydrocephalus
Myelomeningocele assoc with pedunculated choroid
CT more reliable than US for Dx
D/D - Choroid Papilloma, very rare, consider if CSF clear on tap
all assoc with hydrocephalus, enhance intensely on CT
HEMORRHAGIC NEOPLASMS & CYSTS
1. Malignancy Related Coagulopathy - esp with leukemia & chemotherapy
systemic neoplasms can be assoc with term coagulopathy
2. Intratumoral Hematomas - 10%, malignant , Astrocytoma’s are most common.
Neovascularity, central necrosis, plasminogen activators etc contribute
Heterogeneous, incomplete hemosiderin ring, edema persist
multiple lesions & min edema suggests nonneoplastic cause
Cysts & slow growing cystic neoplasm like cranio rarely bleed
Oligodendroglioma, neuroectodermal & teratoma hemorrhage frequently
Ependymoma & choroid tumors - frequent SAH & hemosiderosis
Pituitary Adenoma - may bleed more frequently than astrocytoma
Lymphoma rarely bleed unless with AIDS
Renal cell Ca, chorio Ca, melanoma, thyroid & lung mets, 15%
3. Nonneoplastic Hemorrhagic Cysts -rare, colloid cysts never bleed
Rathke cleft cysts & Arachnoid cysts more commonly bleed
Arachnoid cysts bleed secondary to trauma, bridging vessels rupture
sometimes assoc with subdural hematoma
MISCELLANEOUS CAUSES OF BENIGN INTRACRANIAL HEMORRHAGE
1. Amyloid Angiopathy – Most common cause of bleed in elderly patient with no HTN
nonbranching fibrillar protiens form beta-pleated sheets
Deposit is Cortical & leptomeningeal vessels
extend from small vessels to brain parenchyma
Contractile elements replaced by the crystals
Multiple hematomas frequent & occurs at cortico medullary junction
basal ganglia & brainstem not affected
2. Infection & vasculitis - rare, increased chance if immuncompromised
septic emboli - mycotic aneurysms & hemorrhagic infarct
10% of Infective endocarditis have SAH or parenchymal
Aspergillosis & other fungi directly invade vessel
Thrombosis, infarction & hem result
Herpes Simplex II - the only encephalitis assoc with hematoma
3. Recreational Drugs - 50% have preexisting AVM or aneurysm
Cocaine can induce an acute hypertensive episode, vasospasm
also enhances platelet aggregation, dural sinus thrombosis
amphetamine & PCP also associated with hemorrhage
endothelial damage & necrotizing vasculitis
4. Blood Dyscrasias & Coagulopathies - iatrogenic or acquired
Vit K deficiency, hepatocellular diseases, antibody against clot, DIC
Anticoagulants, thrombolytics, aspirin, Etoh abuse, chemo
15% of all intracranial hemorrhage on anticoagulants
Supratentorial, intraparenchymal bleeds most common
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