The versatile Computed Tomography (CT) has transformed medicine by allowing cross-sectional images of the human body in greater detail than rudimentary X-ray machines, particularly in emergency settings. Depending on the tissue density, the degree of absorption of the electromagnetic waves confers different gradient images. Certain conditions tend to produce high-signal density (brightness) on CT, such as calcification, intracerebral hemorrhage, highly dense tumors, and vascular stasis. Therefore, hyperdensity on a noncontrast CT (NCCT) of the head is not synonymous with hemorrhage, and recognizing distinguishing features could affect management. This article reviews the fundamental knowledge behind Computed Tomography and its application in detecting intraparenchymal hyperdense abnormalities.

The electromagnetic X-rays at a normal wavelength of 0.01 - 10 nanometers exert energies in the range of 100 eV to 100 keV (Figure 1). This short wavelength allows the rays to penetrate and be absorbed based on the tissue’s density, thickness, and atomic number, from the lowest density, such as air-filled lungs, to fat, muscles, and bones [1]-[3] (Table 1). The degree of suppression (or attenuation) at which X-ray beams reach the detectors in a gantry on the other side of a tissue carries a numerical value called the attenuation coefficient, which allows a computer to reconstruct and display the image (tomography). The final data from the attenuation coefficients is rescaled and quantified into linear CT integers from +1000 (compact bone) to −1000 (air), expressed as Hounsfield units (HU), in relation to the attenuation coefficient of water set at 0 HU, with the multiplication factor of 10³ (Figure 2) [4].

Table 1. Densities of various tissues in grams/Liter.

The average density of tissue organs in gm/L. Adapted from The Foundation for Research on Information Technologies in Society (IT’IS), the Swiss Federal Institute of Technology (ETH), Zurich. CSF = cerebrospinal fluid.

Figure 1. The electromagnetic spectrum. Visible light falls in the middle of the visible spectrum. Higher frequency and lower wavelength X-rays and gamma rays possess the highest energy within the electromagnetic spectrum. Computed Tomography (CT) uses X-rays, and Positron Emission Tomography (PET) uses gamma rays.

Figure 2. Hounsfield units and CT number integers.

The density and thickness between two adjacent tissues provide useful information in identifying the nature and structure of an abnormality. Contrast agents, such as iodine, temporarily modify the density for improved visualization. The thinner the slices, the less volume averaging effects where normal and pathological tissues coexist.

Intracerebral hemorrhages (ICH) comprise 13% to 15% of all strokes. Approximately half of patients with ICH will die within one year, and 2/3 of the survivors will acquire significant functional dependency [5]-[7].

Using contemporary digital scanners, the sensitivity of non-contrast CT for subarachnoid hemorrhage is greater than 93% and the specificity is nearly 100%, similar to artificial intelligence and computer vision techniques such as deep learning programming [8]-[10]. The sensitivity and specificity for hemorrhage are the highest within the first 5 days from the onset of symptoms, as the oxyhemoglobin decomposes into deoxyhemoglobin and methemoglobin [11][12]. The central part of an acute intraparenchymal hemorrhage may have an average HU of 67 in the first 2 hours of onset. As the hemoglobin molecule degrades over time, HU drops to 64.5 between the first 12 and 24 hours, and further reduces to 53 HU after 72 hours [13]. The initial high attenuation decreases by approximately 1.5 HU per day, becoming isodense (similar density to the brain parenchyma) within 1 - 6 weeks. This characteristic decrease in attenuation over time is a core distinguishing feature between an acute hemorrhage and other hyperdense lesions, such as calcification or certain tumors.

The location of hyperdensity can indicate certain pathological causes (Table 2). For example, a “Middle Cerebral Artery sign” (Figure 3) whereby the MCA is hyperdense in a large vessel obstructive stroke may also be seen in hemochromatosis [14][15]. To differentiate between the two, HU to serum hematocrit level could be helpful (see discussion). As a general rule, lesions of 60 to 90 HU indicate hemorrhage, whereas those above 100 HU indicate calcification. The normal Hounsfield units for non-occluded blood range from +40 to +43 (mean 41.3), making them isodense or marginally hyperdense with respect to the normal gray matter at +39 HU, and the attenuation of an occlusive thrombus is in the range of 47 to 61 (mean 54.0) HU [16]-[18]. A “dot” or Sylvian fissure sign represents on a non-contrast head CT an occlusion of one or more distal branches of a large intracranial vessel, particularly the MCA (Figure 4), which typically produces a stroke in the insula [19]. Because of a smaller territory infarct attributed to the distal branches, the prognosis is more favorable. Other extra-parenchymal hyperdensities could be found in the sella turcica [20], dural calcification in the form of meningioma [21], craniopharyngioma [22], and lobulated blastoma within the pineal gland, which creates communicating hydrocephalus [23]. The high metabolism within the basal ganglia makes it susceptible to carbon monoxide poisoning [24], hypoxemia, and severe hyperglycemia [25]. Other conditions that affect the basal ganglia comprise the autosomal dominant Primary Familial Brain Calcification (PFGC) or the secondary Fahr’s disease [26], connective tissue disease such as systemic lupus erythematosus [27][28], and HIV [29]. The mechanism is believed to be the result of microinfarctions from immune-mediated vasculopathy. The ventricles can host a variety of rare tumors that include metastases, papillomas and ependymomas, and colloid cysts, with symptoms related to hydrocephalus such as headaches, vomiting, visual obscuration, and ataxia.

Intraparenchymal hemorrhage (IPH) is bleeding inside the brain tissue (parenchyma), often from hypertension or amyloid angiopathy, causing focal neurological deficits like weakness or speech issues, while subarachnoid hemorrhage (SAH) is bleeding into the space around the brain, between arachnoid and pia mater, usually from a ruptured aneurysm, presenting as a sudden, severe headache, nuchal rigidity, and photophobia. IPH involves direct brain tissue damage and swelling, whereas SAH affects the cerebrospinal fluid (CSF) spaces. Both are severe hemorrhagic strokes with distinct locations, causes, and typical symptoms.

Table 2. Etiology of Extra-parenchymal Hyperdensity.

Figure 3. Middle cerebral artery hyperdense sign. A 90+ y/o who awoke with right hemiparesis, left gaze deviation, aphasia and NIHSS of 24. The left image reveals a hyperdense left middle cerebral artery sign (arrows); CT angiography (middle and far right images) shows a left M1 branch occlusion.

Figure 4. “Dot” sign of the left Middle Cerebral Artery (MCA). An 85-y/o patient who, after a fall, was noticed to be nonverbal and with right hemiparesis. CT (left image) and CTA (middle) show the “dot sign” (arrows) with flow void in the M2 branch of the Left MCA. There is hyperdensity on diffusion-weighted images (DWI) in the left insula (right).

Several different conditions may exhibit attenuation on head CT and may mimic hemorrhagic stroke in presentation. They include superficial siderosis, lymphoma, tuberculoma and other infectious causes, metastasis (melanoma, renal cell carcinoma, thyroid carcinoma, choriocarcinoma), vascular malformation such as cavernoma, cerebral amyloid angiopathy, high-grade glioma, and aneurysm. For the sake of simplicity, the mnemonic “SLIM VAGA” can assist in recognizing the most common etiologies. Table 3 provides clinical pearls and references for each condition, followed by case examples.

The distinguishing clinical features of superficial siderosis (Figure 5) include the triad of dysacusis (diminished hearing), with progressive ataxia and dysarthria due to an accelerated ferritin synthesis in the Bergmann glia of the cerebellum [30][31]. The high cellularity of Primary B-cell CNS lymphoma causes high-signal density on CT as well as diffusion-weighted images on the brain MRI (Figure 6). With the application of contrast medium, a homogeneous uptake is observed in most lymphomatous lesions [32][33].

Many infectious agents produce intraparenchymal signal changes on head CT. Common infections include tuberculoma, toxoplasmosis, empyema, and septic emboli [34]. Figure 7 illustrates Staphylococcus endocarditis with embolism to the brain.

Table 3. Etiology of Intra-parenchymal Hyperdensity.

Figure 5. Superficial siderosis. A 60-y/o patient presents with progressive decline in memory and hearing for 6 years, episodic vertigo and disequilibrium for 2 years, and a sudden onset of “Novocain-like” paresthesia in the right side of the lips, cheek and right hand. CT (left) demonstrates hyperdensity in the left central sulcus, not seen on diffusion-weighted images (DWI). Susceptibility-weighted image (SWI) reveals multiple areas of superficial siderosis and hemosiderin deposits.

Figure 6. Lymphoma. A 75-y/o with dizziness and slurred speech. Brain biopsy was c/w diffuse large B-cell lymphoma, FISH negative for BCL2, BCL6, and MYC rearrangements. CT chest/abdomen/pelvis revealed no evidence of systemic lymphoma. CT of the head (left) shows hyperattenuation within the right cerebellar peduncle, and homogenous contrast enhancement (right) on the cranial MRI.

Figure 7. Infectious etiology—Staphylococcus endocarditis. A 60+ y/o who presented with fevers, headache, rash, and weakness for a day secondary to severe sepsis and methicillin-sensitive Staphylococcus aureus bacteremia and a small vegetation over the prosthetic aortic valve. Hyperdensity in the right parietal area on head CT (arrow) with corresponding changes on the FLAIR sequences (right).

Because of their predilection for the vascular border zone regions of the gray and white matter junction, most metastases cannot be detected on non-contrast head CT. The most common hemorrhagic conversions of metastases in the brain are melanoma (Figure 8), renal cell carcinoma, choroid carcinoma, and thyroid carcinoma [35][36]. The mnemonic “MR/CT” might help recall these carcinomas. About 10% of metastatic tumors may present as intracerebral hemorrhage.

Figure 8. Metastatic melanoma. A 75-y/o with 3 weeks of right-sided weakness, unable to bear weight due to right leg buckling. The patient was unable to write with the dominant right hand. (A) CT demonstrates hyperdensity (arrows) with surrounding vasogenic edema, and (B) mostly homogeneous enhancement on brain MRI.

Vascular anomalies, particularly arteriovenous malformation and cavernous hemangioma, can be seen as the “caput medusa” sign in the former (Figure 9), or a heterogeneous “Popcorn” sign in the latter (Figure 10) [37].

Figure 9. Venous malformation. A 20-y/o presents with first seizure. Non-contrast head CT shows a bright density in the right frontoparietal region (top left). With contrast, an irregular enhancing streak is seen with the feeding vasculature on axial (top right). This is better viewed on a brain MRI (bottom left), showing a mixed vascular malformation composed of a 1.1 cm cerebral cavernous venous malformation and an adjacent developmental venous anomaly. CT angiography of the same lesion (arrow) is illustrated.

Figure 10. Cavernoma. A 68-y/o with HTN, developed minutes of immobility in the right hand and fingers when attempting to open the refrigerator door, associated with left-sided headache. A subtle hyperdensity is observed on head CT (white circle), corresponding with changes on the FLAIR (middle), and SWI (arrow).

The sensitivity of head CT in detecting intracerebral aneurysms of all types, fusiform, saccular, or pseudoaneurysm, increases with sizes greater than 7 mm (Figure 11), especially as they exert mass effect on the surrounding parenchymal structures. Most outpouching occurs at bifurcation or trifurcation arterial branches, specifically along the circle of Willis. Most saccular (dome-shaped) aneurysms are secondary to prolonged hypertension, illicit drugs, smoking, and collagen vascular diseases. Up to 30% may occur in multiple areas [38][39].

Figure 11. Aneurysm. A 50-y/o patient with idiopathic seizure disorder as a teenager for a year, who complained of multiple syncopal events that led to a motor vehicle collision and the discovery of a basilar aneurysm. Minimal hyperdensity is seen in the basilar artery on non-contrast CT (white arrow), becoming more noticeable on CT angiography (right image).

Like lymphoma, grade III and IV gliomas can contain areas of high attenuation on the head CT due to its hypercellularity mixed with necrotic tissue (Figure 12). Intra-tumor hemorrhage from a rapidly developing vasculature supply to the tumor is also possible [40][41].

Figure 12. High-grade glioma. A 60+ y/o patient presented with an acute onset of speech disturbance while at work. The exam showed paraphasic errors, disorientation, dyscalculia, and body agnosia. In the left image, CT demonstrated hyperdensity in the superior left frontal-temporal region without enhancement, resembling subarachnoid hemorrhage (green circle). Diffusion-weighted images (inserts to the right) showed hyperintensity in the left temporoparietal lobes and bilateral thalami. Pathology yielded IDH wild-type glioblastoma.

Finally, in individuals older than 60 years of age, the combination of subdural, subarachnoid, and intraventricular hemorrhages simultaneously or spread over time should raise the index of suspicion for primary cerebral amyloid angiopathy [42][43]. Figure 13 demonstrates a case of an 80-year-old person with amyloid angiopathy.

Figure 13. Primary cerebral amyloid angiopathy. An 80-y/o with ICH separated in time and location. CT scans performed on the left when the patient presented with Parkinsonian features, gait difficulty and progressive confusion, compared with 7 months later when more noticeable abrupt confusion was noted (second image from the left), arriving at the physical therapy appointment without shoes and not following instructions. MRI scans taken two years apart show progression of hemosiderin deposits on SWI in both hemispheres, with enlargement of the ventricles (as shown in the two images to the right).

A noncontrast head CT can provide vital information in the acute setting. Depending on different intracranial tissue densities, the high-energy photons (X-rays) emitted by the CT scanner are absorbed linearly—the higher the density, the greater the absorption of X-rays. This is called the attenuation coefficient, which correlates with a mathematical notation known as the Hounsfield unit. Certain conditions tend to produce high-signal density on CT, such as calcification, intracerebral hemorrhage, highly dense tumors, and vascular stasis. When red blood cells degrade, the hemoglobin protein complex absorbs X-rays and leaves a white pixel similar to bone on the detector. The attenuation of the cortex ranges from 37 to 45 HU and less than 15 HU for the cerebrospinal fluid (CSF) spaces. Acute hemorrhage attenuates at 60 - 90 HU and is linearly related to the hematocrit and hemoglobin. Based on the value of the HU, the location of the abnormality, whether it is intra- or extraaxial, and the clinical context, one can determine the etiology with a good degree of certainty. Figure 14 demonstrates an algorithm that can be used to assess some of these etiologies. Calcified lesions possess a HU greater than 100. Those that fall within 60 - 90 HU can further be separated as intra-parenchymal or extra-parenchymal, with further clue by the shape and location of the lesion. A linear hyperdensity may represent a vascular thrombosis if the HU to hematocrit ratio is greater than 1.64 [44]. Otherwise, hemochromatosis or nonketotic hyperglycemia could be considered. Nodular lesions may include metastases, infectious emboli and venous malformations. Diffuse hyperdense lesions on NCCT are ominous for primary brain tumors such as large B-cell lymphoma and high-grade glioma.

Figure 14. Algorithm to assist in identifying different etiologies for HU 60 - 90. Hyperdensity seen on a NCCT can be divided into whether or not the HU is between 60 and 90. If less than 60, the abnormality will blend within the parenchyma, having a HU of 20 - 40. Anything above 100 would indicate calcification, and depending on the location, etiologies vary. When a linear hyperdensity is observed, a HU to hematocrit ratio (HU:Htc) of >1.64 indicates a high sensitivity for a vascular thrombosis. A higher hematocrit, such as seen in hemochromatosis, will lower the ratio even though seen as hyperattenuation on the head CT. Diffuse hyperdense lesions on NCCT may represent intracranial primary tumors. The recommended follow-up imaging studies are displayed in gray boxes. Legend: CO—carbon monoxide; CT—computed tomography; CTA—CT angiography; HIV—human immunodeficiency virus; HU—Hounsfield unit; ICH—intracerebral hemorrhage; IVH—intraventricular hemorrhage; mets—metastatic disease; MRI +/−—magnetic resonance imaging with/without contrast; NCCT—noncontrast CT; SAH—subarachnoid hemorrhage; SDH—subdural hemorrhage; SLE—systemic lupus erythematous; Toxo—toxoplasmosis.

In general, the utility of head CT is indispensable in detecting hemorrhage in the acute setting, particularly within the first 6 - 12 hours, having exceptional sensitivity but low specificity for vascular etiologies. Other conditions that create hyperdensity in the parenchyma may be mistaken for acute hemorrhagic stroke, especially if the presentation is sudden. The mnemonic SLIM VAGA that represents the diagnoses of superficial siderosis, lymphoma, infection, metastases, vascular anomalies, aneurysm, glioma, and amyloid angiopathy may assist in formulating a differential diagnosis when the appearance of blood on CT is questionable. Higher cellularity, vascular or tumoral calcification, and non-pathologic beam-hardening artifact have the potential for producing hyperdensity.

Dual-energy CT can distinguish causes other than intracerebral hemorrhage, but it is not universally available. Non-contrast CT complements other imaging modalities that include digital subtraction angiography, positron emission tomography, and magnetic resonance.

Potential pitfalls to the “60 - 90 HU = hemorrhage; >100 HU = calcification” rule include beam hardening artifact, high hematocrit/polycythemia, contrast staining if prior contrast exists, and calcified tumors.