Head Computed TomographySubagia Santoso SudjonoDepartement of RadiologyGatot Subroto Central Army Hospital*

Technique The patient is placed on the CT table in a supine position and the tube rotates around the patient in the gantry. In order to prevent unnecessary irradiation of the orbits and especially the lenses, Head CTs are performed at an angle parallel to the base of the skull. Intravenous contrast is not routinely used, but may be useful for evaluation of tumors, cerebral infections, and in some cases for the evaluation of stroke patients. *

Slicing in CT Scan*

Anatomy Cranial cross-sectional anatomy is very important to know prior to analyzing a head CT. Once the normal structures are identified, abnormalities can be detected and a diagnosis may be possible. Symmetry is an important concept in anatomy and is almost always present in a normal head CT unless the patient is incorrectly positioned with the head cocked at an angle. *

A. OrbitB. Sphenoid SinusC. Temporal LobeD. External Auditory CanalE. Mastoid Air CellsF. Cerebellar Hemisphere*

A. Frontal LobeB. Frontal Bone (Superior Surface of Orbital Part)C. Dorsum SellaeD. Basilar ArteryE. Temporal LobeF. Mastoid Air CellsG. Cerebellar Hemisphere*

A. Frontal LobeB. Sylvian FissureC. Temporal LobeD. Suprasellar CisternE. MidbrainF. Fourth VentricleG. Cerebellar Hemisphere*

A. Falx CerebriB. Frontal LobeC. Anterior Horn of Lateral VentricleD. Third VentricleE. Quadrigeminal Plate CisternF. Cerebellum*

A. Anterior Horn of the Lateral VentricleB. Caudate NucleusC. Anterior Limb of the Internal CapsuleD. Putamen and Globus PallidusE. Posterior Limb of the Internal CapsuleF. Third VentricleG. Quadrigeminal Plate CisternH. Cerebellar VermisI. Occipital Lobe*

A. Genu of the Corpus CallosumB. Anterior Horn of the Lateral VentricleC. Internal CapsuleD. ThalamusE. Pineal GlandF. Choroid PlexusG. Straight Sinus*

A. Falx CerebriB. Frontal LobeC. Body of the Lateral VentricleD. Splenium of the Corpus CallosumE. Parietal LobeF. Occipital LobeG. Superior Sagittal Sinus*

A. Falx CerebriB. SulcusC. GyrusD. Superior Sagittal Sinus*

TRAUMA*

Skull fractures are categorized as linear or depressed, depending on whether the fracture fragments are depressed below the surface of the skull. Linear fractures are more common. The bone windows must be examined carefullyA skull fracture is most clinically significant if the paranasal sinus or skull base is involved.*

Skull Fractures Fractures must be distinguished from sutures that occur in anatomical locations (sagittal, coronal, lambdoidal) and venous channels. Sutures have undulating margins both sutures and venous channels have sclerotic margins. Venous channels have undulating sides. Depressed fractures are characterized by inward displacement of fracture fragments. *Linear skull fracture of the right parietal bone (arrows).

Subarachnoid Hemorrhage *High density blood (arrowheads) fills the sulci over the right cerebral convexity in this subarachnoid hemorrhage.

Acute Subdural Hematoma Deceleration and acceleration or rotational forces that tear bridging veins can cause an acute subdural hematoma. The blood collects in the space between the arachnoid matter and the dura matter. The hematoma on CT has the following characteristics: - Crescent shaped - Hyperdense, may contain hypodense foci due to serum, CSF or active bleeding - Does not cross dural reflections *

High density, crescent shaped hematoma (arrowheads) overlying the right cerebral hemisphere. Note the shift of the normally midline septum pellucidum due to the mass effect arrow. *The hypodense region (arrow) within the high density hematoma (arrowheads) may indicate active bleeding.

Subacute Subdural Hematoma Subacute SDH may be difficult to visualize by CT because as the hemorrhage is reabsorbed it becomes isodense to normal gray matter. A subacute SDH should be suspected when you identify shift of midline structures without an obvious mass. Giving contrast may help in difficult cases because the interface between the hematoma and the adjacent brain usually becomes more obvious due to enhancement of the dura and adjacent vascular structures. Some of the notable characteristics of subacute SDH are: - Compressed lateral ventricle - Effaced sulci - White matter "buckling" - Thick cortical "mantle" *

Subacute subdural hematoma (arrowheads). Note the compression of gray and white matter in the left hemisphere due to the mass effect. *

Chronic Subdural Hematoma Chronic SDH becomes low density as the hemorrhage is further reabsorbed. It is usually uniformly low density but may be loculated. Rebleeding often occurs and causes mixed density and fluid levels. *

*Crescent shaped chronic subdural hematoma (arrowheads). Notice the low attenuation due to reabsorbtion of the hemorrhage over time. This chronic subdural hematoma (arrowheads) shows the septations and loculations that often occur over time.

Epidural Hematoma An epidural hematoma is usually associated with a skull fracture. It often occurs when an impact fractures the calvarium. The fractured bone lacerates a dural artery or a venous sinus. The blood from the ruptured vessel collects between the skull and dura. On CT, the hematoma forms a hyperdense biconvex mass. It is usually uniformly high density but may contain hypodense foci due to active bleeding. Since an epidural hematoma is extradural it can cross the dural reflections unlike a subdural hematoma. However an epidural hematoma usually does not cross suture lines where the dura tightly adheres to the adjacent skull. *

Biconvex (lenticellular) epidural hematoma (arrowheads), deep to the parietal skull fracture (arrow). *

Diffuse Axonal Injury Diffuse axonal injury is often referred to as "shear injury". It is the most common cause of significant morbidity in CNS trauma. Fifty percent of all primary intra-axial injuries are diffuse axonal injuries.

The CT of a patient with diffuse axonal injury may be normal despite the patient's presentation with a profound neurological deficit. With CT, diffuse axonal injury may appear as ill-defined areas of high density or hemorrhage in characteristic locations. The injury occurs in a sequential pattern of locations based on the severity of the trauma.

The following list of diffuse axonal injury locations is ordered with the most likely location listed first followed by successively less likely locations: - Subcortical white matter - Posterior limb internal capsule - Corpus callosum - Dorsolateral midbrain *

*Hemorrhage of the posterior limb of the internal capsule (arrow) and hemorrhage of the thalamus (arrowhead). Hemorrhage in the corpus callosum (arrow).

Cerebral Contusion Cerebral contusions are the most common primary intra-axial injury. They often occur when the brain impacts an osseous ridge or a dural fold. The foci of punctate hemorrhage or edema are located along gyral crests. The following are common locations: - Temporal lobe - anterior tip, inferior surface, sylvian region - Frontal lobe - anterior pole, inferior surface - Dorsolateral midbrain - Inferior cerebellum.On CT, cerebral contusion appears as an ill-defined hypodense area mixed with foci of hemorrhage. Adjacent subarachnoid hemorrhage is common. After 24-48 hours, hemorrhagic transformation or coalescence of petechial hemorrhages into a rounded hematoma is common. *

Multiple foci of high density corresponding to hemorrhage (arrows) in an area of low density (arrowheads) in the left frontal lobe due to cerebral contusion. *

Intraventricular Hemorrhage Traumatic intraventricular hemorrhage is associated with diffuse axonal injury, deep gray matter injury, and brainstem contusion. An isolated intraventricular hemorrhage may be due to rupture of subependymal veins. *Intraventricular hemorrhage (arrow) found in a trauma patient. Note the subarachnoid hemorrhage in the sulci in the subarachnoid space (arrowheads).

STROKE*

Stroke Subtypes Strokes are classified into two major types - hemorrhagic and ischemic. Hemorrhagic strokes are due to rupture of a cerebral blood vessel that causes bleeding into or around the brain. Hemorrhagic strokes account for 16% of all strokes. An ischemic stroke is caused by blockage of blood flow in a major cerebral blood vessel, usually due to a blood clot. Ischemic strokes account for about 84% of all strokes. Ischemic strokes are further subdivided based on their etiology into several different categories including thrombotic strokes, embolic strokes, lacunar strokes and hypoperfusion infarctions. *

Hemorrhagic Stroke Hemorrhagic strokes account for 16% of all strokes. There are two major categories of hemorrhagic stroke. Intracerebral hemorrhage is the most common, accounting for 10% of all strokes. Subarachnoid hemorrhage, due to rupture of a cerebral aneurysm, accounts for 6% of strokes overall. *Hemorrhage in the cerebellum (arrow).

Intracerebral Hemorrhage The most common cause of non-traumatic intracerebral hematoma is hypertensive hemorrhage. Other causes include amyloid angiopathy, a ruptured vascular malformation, coagulopathy, hemorrhage into a tumor, venous infarction, and drug abuse. *Thalamic hemorrhage (arrow) extending into the left lateral ventricle (arrowheads).

Hypertensive Hemorrhage Hypertensive hemorrhage accounts for approximately 70-90% of non-traumatic primary intracerebral hemorrhages. It is commonly due to vasculopathy involving deep penetrating arteries of the brain. Hypertensive hemorrhage has a predilection for deep structures including the thalamus, pons, cerebellum, and basal ganglia, particularly the putamen and external capsule. Thus, it often appears as a high-density hemorrhage in the region of the basal ganglia. Blood may extend into the ventricular system. Intraventricular extension of the hematoma is associated with a poor prognosis. *Hypertensive hemorrhage in the basil ganglia.

Coagulopathy Related Intracerebral Hemorrhage Coagulopathy related intracerebral hemorrhage can be due to drugs such as coumadin or a systemic abnormality such as thrombocytopenia. On imaging, this hemorrhage often has a heterogeneous appearance due to incompletely clotted blood. A fluid level within a hematoma suggest coagulopathy as an underlying mechanism. *Notice the fluid level within the hematoma (arrow).

Hemorrhage Due to Arteriovenous Malformation An underlying arteriovenous malformation (AVM) may or may not be visible on a CT scan. However, prominent vessels adjacent to the hematoma suggest an underlying arteriovenous malformation. In addition, some arteriovenous malformations contain dysplastic areas of calcification and may be visible as serpentine enhancing structures after contrast administration. *

*The CT on the left shows hemorrhage (arrow) due to underlying AVM (arrowheads). The arteriogram on the right shows the tangle of vessels (arrowheads) of the AVM. This lesion would be considered for intravascular embolic therapy.

Subarachnoid Hemorrhage In the absence of trauma, the most common cause of subarachnoid hemorrhage is a ruptured cerebral aneurysm. Cerebral aneurysms tend to occur at branch points of intracranial vessels and thus are frequently located around the Circle of Willis. Common aneurysm locations include the anterior and posterior communicating arteries, the middle cerebral artery bifurcation and the tip of the basilar artery. Subarachnoid hemorrhage typically presents as the "worst headache of life" for the patient. Detection of a subarachnoid hemorrhage is crucial because the rehemorrhage rate of ruptured aneurysms is high and rehemorrhage is often fatal.*

CT is currently the imaging modality of choice because of its high sensitivity for the detection of subarachnoid hemorrhage. CT is most sensitive for acute subarachnoid hemorrhage. After a period of days to weeks CT becomes much less sensitive as blood is resorbed from the CSF. If there is a strong clinical indication, LP may be warranted despite a negative CT since small bleeds can be unapparent on imaging.On CT, a subarachnoid hemorrhage appears as high density within sulci and cisterns. The insular regions and basilar cisterns should be carefully scrutinized for subtle signs of subarachnoid hemorrhage. Subarachnoid hemorrhage may have associated intraventricular hemorrhage and hydrocephalus.

*

High density blood fills the cisterns (arrowheads) in this patient with hemorrhage from the left middle cerebral artery. Note the middle cerebral artery aneurysm (arrows). *

Ischemic stroke Ischemic strokes are caused by thrombosis, embolism of thrombosis, hypoperfusion and lacunar infarctions. A thrombotic stroke occurs when a blood clot forms in situ within a cerebral artery and blocks or reduces the flow of blood through the artery. This may be due to an underlying stenosis, rupture of an atherosclerotic plaque, hemorrhage within the wall of the blood vessel, or an underlying hypercoagulable state. This may be preceded by a transient ischemic attack and often occurs at night or in the morning when blood pressure is low. Thrombotic ischemic strokes account for 53% of all strokes.An embolic stroke occurs when a detached clot flows into and blocks a cerebral artery. The detached clot often originates from the heart or from the walls of large vessels such as the carotid arteries. Atrial fibrillation is also a common cause. Embolic strokes account for 30% of all strokes. *

A lacunar infarction occurs when the walls of small arteries thicken and cause the occlusion of the artery. These typically involve the small perforating vessels of the brain and result in lesions that are less than 1.5 cm in size.Hypoperfusion infarctions occur under two circumstances. Global anoxia may occur from cardiac or respiratory failure and presents an ischemic challenge to the brain. Tissue downstream from a severe proximal stenosis of a cerebral artery may undergo a localized hypoperfusion infarction. Lacunar and hypoperfusion strokes, account for the remaining 1% of strokes of the ischemic type*

Imaging of Stroke "Stroke" is a clinical diagnosis; however imaging is playing an increasingly important role in its diagnosis and management. The most important issue to determine when imaging a stroke patient is whether one is dealing with a hemorrhagic or ischemic event. This has crucial therapeutic and triage implications. Decisions that must be made concerning therapy are dependent on the diagnosis and may include the following: - Is the patient a thrombolysis candidate and should thrombolytic therapy be used? - Intravenous or intrarterial therapy? - Neurosurgery or neurology patient? In addition about 2% of clinically definite "strokes" are found to be a result of some other pathology such as a tumor, a subdural hematoma or an infection. *

CT scanning There are several advantages to performing a CT scan instead of other imaging modalities. A CT scan: - Is readily available - Is rapid - Allows easy exclusion of hemorrhage - Allows the assessment of parenchymal damage The disadvantages of CT include the following: - Old versus new infarcts is not always clear - No functional information (yet) - Limited evaluation of vertebrobasilar system A CT is 58% sensitive for infarction within the first 24 hours (Bryan et al, 1991). MRI is 82% sensitive. If the patient is imaged greater than 24 hours after the event, both CT and MR are greater than 90% sensitive. *

CT Pathophysiology After a stroke, edema progresses, and brain density decreases proportionately. Severe ischemia results in a 3% increase in intraparenchymal water within 1 hour. This corresponds to 7-8 Hounsfield Unit decrease in brain density. There is also a 6% increase in water at 6 hours. The degree of edema is related to the severity of hypoperfusion and the adequacy of collateral vessels. *Sharply circumscribed hypodense edema (arrowheads) in the right middle cerebral artery territory.

CT Findings of Stroke When analyzing the CT of a potential stroke victim, one of the first findings to look for is the presence or absence of hemorrhage. Another common finding in stroke patients is a dense middle cerebral artery or a dense basilar artery, which corresponds to thrombus in the affected vessel. There are also more subtle changes of acute ischemia due to edema which include the following: - Obscuration of the lentiform nuclei - Loss of insular ribbon - Loss of gray/white distinction - Sulcal effacement *

*Dense basilar artery (arrow).

Hyperdense Vessel Sign A hyperdense vessel is defined as a vessel denser than its counterpart and denser than any non-calcified vessel of similar size. This is seen in 25% of stroke patients. In patients presenting with clinical deficit referable to the middle cerebral artery territory, the hyperdense vessel sign is present 35-50% of the time. *High density in the right middle cerebral artery (arrowheads). Compare it with the normal left middle cerebral artery (arrow).

Basilar Thrombosis Thrombosis of the basilar artery is a common finding in stroke patients. CT findings include a dense basilar artery without contrast injection. *Dense basilar artery (arrow). Compare this to the normal internal carotid artery (arrowhead).

Lentiform Nucleus Obscuration Lentiform nucleus obscuration is due to cytotoxic edema in the basal ganglia. This sign indicates proximal middle cerebral artery occlusion, which results in limited flow to lenticulostriate arteries. Lentiform nucleus obscuration can be seen as early as one hour post onset of stroke. *Hypodensity in the left hemisphere (arrows) involving the caudate nucleus and lentiform nuclei (globus pallidus and putamen).

Insular Ribbon Sign The insular ribbon sign is the loss of the gray-white interface in the lateral margins of the insula. This area is supplied by the insular segment of the middle cerebral artery and is particularly susceptible to ischemia because it is the most distal region from either anterior or posterior collaterals. The insular ribbon sign may involve only the anterior or the posterior insula. *The cortex of the left insular ribbon is not visualized (arrow).

Diffuse Hypodensity and Sulcal Effacement Diffuse hypodensity and sulcal effacement is the most consistent sign of infarction. Extensive parenchymal hypodensity is associated with poor outcome. If this sign is present in greater than 50% of the middle cerebral artery territory there is, on average, an 85% mortality rate. Hypodensity in greater than one-third of the middle cerebral artery territory is generally considered to be a contra-indication to thrombolytic therapy.*Hypodensity and sulcal effacement (arrowheads) in the right middle cerebral artery distribution.

CT of Subacute Infarction The CT of a subactue infarction has the following findings in 1 -3 days: - Increasing mass effect - Wedge shaped low density - Hemorrhagic transformation After 4 - 7 days the CT is characterized by: - Gyral enhancement - Persistent mass effect In 1-8 weeks: - Mass effect resolves - Enhancement may persist*

*This image was taken 4 hours after the infarction. This image, from the same patient, was taken 2 days after the infaction.

Enhancement in Infarctions Ninety percent of infarcts enhance on CT examinations with intravenous contrast at 1 week after the infarct. Approximately 35% enhance by 3 days. Faint enhancement begins near the pial surface or near the infarct margins. The enhancement is initially smaller than the area of infarction. It subsequently becomes gyriform. Enhancement is due to breakdown of the blood brain barrier, neovascularity, and reperfusion of damaged brain tissue. *Post contrast CT scan demonstrating gyriform enhancement of subacute right frontal lobe infarct (arrow).

INFECTION*

Meningitis Imaging in suspected meningitis patients is performed to look for complications and assess safety of lumbar puncture. Imaging is not usually performed to diagnose meningitis because imaging studies are frequently normal despite the presence of the disease. *

Complications of Meningitis The following are common complications of meningitis that can be seen using imaging techniques: o Hydrocephalus o Ventriculitis / Ependymitis o Subdural effusion o Subdural empyema o Cerebritis / Abscess o Vasospasm / arterial infarcts o Venous thrombosis / venous infarcts *

Hydrocephalus Hydrocephalus, a problem with the ratio of production of CSF to its reabsorbtion, is most frequent in children. Communicating hydrocephalus is the most common and is due to arachnoid villi and subarachnoid space obstruction. Obstructive hydrocephalus is less common but may occur as a result of the following: o Aqueductal stenosis or occlusion o Trapped fourth ventricle o Ependymitis *

*In these sections from the same patient notice the enlagement of the ventricles and cisterns that occurs with hydrocephalus.

Ventriculitis / Ependymitis Inflammation and enlargement of the ventricles characterizes ventriculitis. Ependymitis shows hydrocephalus with damage to the ependymal lining and proliferation of subependymal glia. A CT of patients with these conditions reveals the presence of periventricular edema and subependymal enhancement. Ventriculitis and Ependymitis affect approximately 30% of the adult patients and 90% of the pediatric patients with meningitis. *In this post contrast CT scan, note the ring enhancing brain abscess (arrowheads) and enhancement of the ependymal lining of the atrium by the left lateral ventricle (arrow).

Cerebrovascular Complications of Meningitis The development of cerebrovascular problems is the most common complication of meningitis. Arterial infarction can occur which often affects the basal ganglia due to the occlusion of small perforating vessels. Hemispheric infarction can also occur due to major vessel spasm. Venous infarctions are also common and can include cortical venous occlusion or the involvement of the superior sagittal sinus. *

The image on the left shows thrombosis of the superior sagittal sinus (arrow) prior to the administration of contrast. The image on the right shows the thrombosis in the same patient after contrast administration. *

Extra-axial CNS Infection Extra-axial CNS infections can involve epidural abscess or subdural empyema. Extra-axial CNS infections account for 20-30% of CNS infections. Fifty percent of extra-axial infections are associated with sinusitis, usually frontal sinusitis. The infection occurs by direct extension or septic thrombophlebitis. Thirty percent of extra-axial infections occur post-craniotomy. Finally, 10-15% of extra-axial CNS infections are related to meningitis. CT findings include a focal fluid collection usually with an enhancing margin in a subdural or epidural location. *

Epidural Abscess On CT, an epidural abscess appears as a focal low-density epidural mass. Dural enhancement may be present as well. The mass may extend into the subgaleal space. It also may cross the midline but usually does not cross suture lines. *

In the left image notice the rim enhancing epdural fluid collection (arrowheads). In the right image, notice the opacification of the left frontal sinus due to acute sinusitis (arrow).*

Subdural Empyema Subdural empyema is usually due to meningitis, sinusitis, trauma or prior surgery. It is a neurosurgical emergency. Subdural empyema leads to rapid clinical deterioration, especially if it is due to sinusitis. On CT it appears as an isodense or hypodense extra-axial mass. It has a lentiform or crescentic shape. The margin of collection often enhances with contrast material administration due to the presence of granulation tissue or subjacent cortical inflammation. *

Notice the heterogeneous subdural fluid collection. In the same patient, post contrast administration, notice the patchy enhancement of the fluid collection.*

*TUMOR

Glioblastoma Multiforme Glioblastoma Multiforme is the most aggressive grade of astrocytoma. The two-year survival rate of patients diagnosed with Glioblastoma Multiforme is 10-15%. On CT, GBM is characterized by necrosis and irregular enhancement. It is one of very few lesions that frequently cross the corpus callosum. *

Notice the ill-defined low density in the right frontal region. An image post contrast administration in the same patient reveals patchy enhancement, a portion of which is crossing the corpus callosum (arrow).*

Meningioma Meningiomas are the most common extra-axial neoplasm of the brain. Middle-aged women are most frequently affected. Twenty percent of meningiomas calcify. On CT, meningiomas are usually isointense to gray matter. *

Bone windows confirm calcification within the mass. Axial, post contrast CT demonstrating broad based enhancing extra-axial mass. *

DEGENERATIVE*

Alzheimer's Disease - Imaging Because of its low sensitivity and specificity for the diagnosis of Alzheimer's disease, imaging is typically not used to rule in Alzheimer's disease but rather to rule out other causes of dementia. Nevertheless, in the right clinical context Alzheimer's disease appears radiographically as diffuse cerebral atrophy with enlarged lateral ventricles and widened sulci on CT. On thin-section (3 mm thick) coronal T1-weighted MR, medial temporal lobe atrophy primarily in the amygdala, hippocampus, and parahippocampal gyrus may be visually evident. Utilizing MR volumetric measurements, the hippocampal formation may be quantitatively determined to show focal atrophy. In addition, the temporal horns, supracellar cisterns, and Sylvian fissures may exhibit focal symmetric or asymmetric enlargement. *

*MR has been chosen for the above images because of its ability to show greater detail in AD. The image on the left is a thin-section coronal T1-weighted MRI of an individual with AD. The arrows indicate focal, assymetric atrophy of the right medial temporal lobe and also visible on the left are the dilated lateral and third ventricles most likely due to diffuse atrophy. The image on the right is an age-matched control for comparison.

Huntington's Disease - Imaging Radiographically Huntingtons disease characteristically exhibits caudate atrophy on imaging. This may be manifested by a decrease in the convexity of the heads of the caudate bilaterally or by an increase in the relative volume of the lateral ventricles as seen on CT or T1-weighted coronal MR. To a lesser extent putaminal atrophy may also be manifested. One method of referencing the degree of caudate atrophy is to use the ratio between intercaudate distance and calvarial width. Known as the bicaudate ratio, the value is found by measuring the minimum distance between the caudate indentations of the frontal horns and the distance between the inner tables of the skull along the same line and multiplying that figure by 100. The Bicaudate Index (BCI) provides a standard by which configured values may be compared to age-matched controls. This parameter has been found to correlate well with caudate atrophy. *

The images above are axial Head CT scans. The image on the left exhibits bilateral caudate head atrophy (red arrowheads), as seen by a decrease in the medial convexities, & lateral ventricle dilatation. Generalized atrophy evident as diffusely widened sulci is also apparent in the image on the left. The image on the right is an age-matched control. *

Pick's Disease - Imaging Radiographically Picks disease, a variant of Frontotemporal dementia, appears as prominent atrophy of the temporal and/or frontal lobes on CT. Sulcal prominence, widening of the Sylvian fissure with atrophy of the insula, inferior frontal and superior temporal lobes, as well as enlargement of the frontal or temporal horns of the lateral ventricles is most evident on MRI. In addition, MR volumetric analysis may show subtle involvement of the orbitofrontal cortex. *

*The images above are axial Head CT scans. In the image on the left, focal bifrontotemporal atrophy can be seen, as exhibited by marked widening of the frontal and temporal sulci, dilation of the lateral ventricles, and the "knife-like" projections of the gyri. The image on the right is an age-matched control for comparison.

*Thank You God Bless

*********************************************************************************