decreased uptake of CSF. The earliest sign oJ this hydrocephalus is oJten dilatittn oJthe temporal fiorns, and the size of these structures must always be evaluatedwhen reading a CT.

A normal CT scan is reassuring but does not absolutely exclude the pres-ence of a subarachnoid hemorrhage if the hemorrhage is extremely small, has

occurred several days previously, or was located low in the posterior fossa orin the spinal axis. In patients in whom there is a high clinical suspicion that theheadache resulted from subarachnoid hemorrhage, a lumbar puncture wouldbe the next examination of choice, looking for small quantities of red bloodcells in the CSF and/or xanthochromia.

Other causes of SAH are bleeding from an arteriovenous malformation(AVM), trauma, hemorrhagic tumor, and dural malformation. The imagesthat follow illustrate the findings of SAH, which may be quite subtle insentinel bleeds.

CT Interpretation in SAH

86 EMEncsNcv CT ScaNs or ruE Hrao: A Pnacrrcal Arlas

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Noncontrast Yersus ContrastCranial CT Scans

In the emergency setting, a noncontrast study should be P^erformed first be-

.urrr" i*po.i"rt i.tfot-u]tion, in particular the presence of acute intracranial

h".o..hug",islostafterintravenouscontrastenharrcement.Contrastcanalways b."ud..tinirtered after the noncontrast study but it is important to re-

memberthattheeffectofcontrastenhancementCannotberemovedformanyhours. Contrast may mask the recognition and delay appropriate treatment of

serious conditions such as subarachnoid or intracerebral hemorrhage, subacute

infarction, or even encePhalitis'In the trauma patient, the sequence of various imaging studies of other body

regionsmustbecarefullyplan,'edtonotobscureacuteintracranialhemor-.ttig. Uy radiographic contrast administered for the other studies'

Lesions enhance with contrast or aPpear to abnorma\ enhance if: (1) the

blood-brain barrier is compromi'"j 1" occurs with neoplasms and ab-

scesses), allowing the contrast material to leak through the capillaries, and

(2) there is increased vascularity and therefore a greater concentration of the

dye, for example, (a) AV malformation or aneurysmal sac and (b) a tumor

.or.rp."rr.. and compacts the normal brain and blood vessels around the

perimeter o[ the lesion.

Analysis of Images

There are many approaches to analysis of a cranial CT scan' We mainly adopt

one that works for us individually, but having adopted an approach it is im-

portant to stick to it for every scan and analyze the visualized structures on

.".h ,1i... Failure to look at all the images results in misinterpretations or im-

portant findings being missed. As in anything else, there is no substitute for

seeing many scans to become proficient'f.,r..i CT scun should be interpreted with the following concePts in mind.

Th"y "r. summarized in the box on page 29 andfurther illustrated and elabo-

rated upon in subsequent chapters'

t.

4 EurncsNcv CT Scaxs or rnr Hneo: A Pnacuca'l Arles

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line)-)cisterna magna. The CSF flows from the cisterna magna over thecerebral convexities and is then absorbed through the arachnoid yilliinto the sagittal sinus, which is a venous structure. Decreased absorptionis due to pathology at the level of the arachnoid villi.

' Hydrocephalus is "active" when the intraventricular pressure is raised,causing progressive enlargement of the ventricles.

' Hydrocephalus is "balanced" or "arrested" when "o*p..rrrtoly mech-anisms allow the intraventricular pressure to return to normal so thatthe ventricles no longer tend to enlarge.

In severe or active hydrocephalus the cortical sulci are effaced (com-pressed). Another feature srrggesting that the intraventricular pressure israised is blunting of the margins of the ventricular system. This is mostpronounced in the area of the temporal horns and these structures ap-pear"ballooned."When the hydrocephalus is active in nature there is alsoevidence offinger-like hypodensities adjacent to the {iontal and occipi-tal horns that result froro transependymalfiow of CSF.

Atrophy Atrophy is a comrnon fi"dirg on many CT scans performedin a busy emergency departrnent because the incidence of neurologics)rmptoms increases with increasing age. Confusion sometimes exists indifferentiating the ventricular enlargement associated with cerebral at-rophy fiom hydrocephalus. In general, cerebral atrophy produces enlarge-ment oJthe cortical sulci and subarachnoid cisterns.This may rcsuh in passive,compensator)l enlargement oJ the venticular system.

Cerebral atrophy is composed of varying proportions of cortical andsubcortical atrophy. Cortical atrophy is predominantly atrophy of the graymatter at the surface of the brain. Subcortical atrophy is predominantlyatrophy of t}e white matter located beneath the cortex. Generally, cor-tical atrophy is associated wit} sulcal enlargement and subcortical atro-phy is associated with ventricular enlargement; however, both areas areinvariably enlarged to a greater or lesser degree.

Remember that in hydrocephalvs therc is disproportionate enlargement oJthe ventricular slstem rclative to the cortical sulci and subarachnoid cisterns.

Cerebral infarction The presence of a cerebral infarction is oftennot evident on CT in the first 12 to 24 hours. However, early in tJrecourse of infarction, subtle mass effect may be appreciated in the area ofinvolvement and this usually manifests as sulcal effacement (compres-

EurncrNcy CT SceNs or rrrs HrRo: A Pnacrrcar, Auas

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cause is warranted if there is no history of recent lumbar puncture orcraniotomy. Air collections usually appear as small droplets located inthe subarachnoid or subdural space.They are often adjacent to a frac-ture of the skull vault or skull base. Intracranial air associated withbasilar skull fractures is due to communication with the mastoid aircells or paranasal sinuses.

Intracranial gas collections result from gas producing microorgan-isms associated with cerebral abscesses and are quite rare. This gas

cannot be distinguished from air collections on CT.

. FatFat appears similar to air on the CT scan but if one were to actuallymeasure its attenuation coefficient it would be higher than air.This can

be done practically to assist with the diagnosis. Intracrarrial fat collec-tions are abnormal and usually associated with benign tumors such as

lipomas or dermoids. Dermoids have a tendency to rupture andspread their contents, in the form of fat droplets, throughout the sub-arachnoid space, frequently inciting a chemical meningitis.

' Gray Matter HypodensitiesCerebral infarctions, after approximately 12 to 2+ hours, producehypodense change in t}e involved gray matter. Recall that there is graymatter in the cortex and t}e basal ganglia and either region may ex-hibit hypodense changes with infarction. Because healthy white mat-ter is normally hypodense (darker) compared to healthy gray matteSwhen infarction causes the gray matter to become hlpodense, it pro-duces a so-called "loss oJ dfferentiation oJ the gray-white inte{ace)'Whencerebral infarctions become chronic there is further decrease in den-sity as encephalomalacia develops.

. White Matter HypodensitiesLow density change confined to the white matter often has a "finger-like" configuration. This is usually the result of disease processes thatcause white matter edema o5 less commonly, white matter ischemiasuch as is seen with leukomalacia secondary to small vessel angiopathyor radiation treatment. There may be local mass effect associated withwhite matter edema. Furt}er investigation of an underlying cause forthis is most conveniendy performed with a contrast enhanced CT scan.

8 EmrncrNcv CT ScaNs or tnr Htao: A Pnecrrcer Arr-es

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