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1.5 Gastrointestinal Hemorrhage 39
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1.5
Gastrointestinal Hemorrhage
Gastrointestinal (GI) bleeding is classically divided
into upper and lower GI bleeding. Upper GI bleeding
is defi ned as bleeding proximal to the ligament of
Treitz, and lower GI bleeding is bleeding distal to the
ligament of Treitz.
Causes of upper GI bleeding include erosions or
ulcers, esophageal varices, Mallory-Weiss tear, and neoplasms. Lower GI bleeding causes include diverticulitis,
ulcerative colitis, angiodysplasia, and neoplasms.
Patients with GI bleeding are often asymptomatic
until blood loss exceeds 100 mL per day. Tachycardia
and hypotension occur when bleeding exceeds 500 mL
per day, and systemic shock develops when >15% of
the circulation blood volume is lost. Symptoms of
upper GI bleeding include vomiting blood (hematemesis) and passing dark stool due to blood digestion
(melena). Severe lower GI bleeding may present with
passing fresh blood (hematochezia). In up to 75% of
upper GI bleeding cases and 80% of lower GI bleeding
cases, the bleeding will stop spontaneously with conservative treatment alone. In the remaining 20–25% of
cases, further intervention is required.
In recent years, the role of multidetector CT in
detecting the source and the cause of bleeding has
increased dramatically. CT-angiography is commonly
performed to detect the source of bleeding due to its
fast scanning time and greater anatomical coverage.
Disadvantages of CT-angiography include radiation
exposure and inability to perform intervention.
In the classical catheter angiography, bleeding rates
as low as 0.5 mL/min can be detected with sensitivity
of 63–90% for upper GI bleeding and 40–86% for
lower GI bleeding. Conventional angiography specifi city of up to 100% is established for both. Active
bleeding is detected by extravasation of the contrast
material into bowel lumen (pathognomonic sign).
Indirect signs of bleeding include detection of aneurysms, arteriovenous fi stula, neovascularity, and
extravasation of the contrast material into confi ned
space. CT-angiography can detect active bleeding rate
as low as 0.3 mL/min.
Signs on CT-Angiography
Active GI bleeding is detected in the arterial phase of the scan
when the contrast material is seen within the bowel lumen
(91–274 HU). The extravasated contrast material may
demonstrate jet-like, linear, swirled, or pooled confi guration
(Fig. 1.5.1 ).
The presence of hyperattenuated material within the bowel
lumen in postcontrast images that was not seen in the
precontrast images is diagnostic of acute GI bleeding (Fig. 1.5.1 ).
For GI bleeding CTA, only intravenous contrast injection is
used. CTA is performed without prior oral administration of
water or contrast material. Water can dilute the extravasated
contrast material, causing false negative results.
Clotted blood attenuation is 28–82 HU, which can be
diff erentiated from active bleeding (>90 HU).
Fig. 1.5.1. Axial abdominal CTA illustration precontrast ( a ) and
postcontrast ( b ). GI bleeding is detected in the arterial phase of
the scan as an extravasation of the contrast material within the
bowel lumen ( arrowhead )
40 Chapter 1 Gastroenterology
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1.5
For Further Reading
1 . Jaeckle T et al Acute gastrointestinal bleeding: value of
MDCT. Abdom Imaging. 2008;33:285–93.
2 . Laing CJ et al Acute gastrointestinal bleeding: emerging
role of multidetector CT angiography and review of current imaging techniques. RadioGraphics. 2007;27:1055–70.
3 . Yoon W et al Acute gastrointestinal bleeding: contrast-
enhanced MDCT. Abdom Imaging. 2006;31:1–8.
4 . Yoon W et al Acute massive gastrointestinal bleeding:
detection and localization with arterial phase multi-detector row helical CT. Radiology. 2006;239:160–67.
5 . Scheffel H et al Acute gastrointestinal bleeding: detection
of source and etiology with multi-detector-row CT. Eur
Radiol. 2007;17:1555–65.
6 . Ha HK et al Radiologic features of vasculitis involving the
gastrointestinal tract. RadioGraphics. 2000;20:779–94.
7 . Ernst O et al Helical CT in acute lower gastrointestinal
bleeding. Eur Radiol. 2003;13:114–17.
8 . Yamaguchi T et al Enhanced CT for initial localization of
active lower gastrointestinal bleeding. Abdom Imaging.
2003;28:634–36.
Chapter 2
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Neurology
CONTENTS
2.1 Stroke (Brain Infarction) 42
2.2 Stroke Diseases and Syndromes 47
2.3 Intracranial Hemorrhage 57
2.4 Meningitis 63
2.5 Encephalitis 67
2.6 Epilepsy 75
2.7 Headache 79
2.8 Multiple Sclerosis and Other Demyelinating Diseases 84
2.9 Parkinsonism 91
2.10 Dementia 93
2.11 Huntington’s Disease 101
2.12 Heat Stroke (Pancerebellar Syndrome) 103
J. A. Al-Tubaikh: Internal Medicine – An Illustrated Radiological Guide
DOI: 10.1007/978-3-642-03709-2_2, © Springer-Verlag Berlin Heidelberg 2010
41
42 Chapter 2 Neurology
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2.1
Stroke (Brain Infarction)
Arterial embolism : the embolus blocks the artery, and
in some times a small hole develops within the embolus
making blood gush into the capillaries with high speed
and pressure, causing them to rupture and bleed.
2.1
Stroke means the death of brain cells (infarction) due
to ischemia or emboli.
The most common causes of stroke are: atherosclerosis, embolic vascular occlusion, hypertension, and
infl ammatory vascular diseases (vasculitis). Patients
present with sudden neurological defi cits in the body
according to the area of the brain affected. Up to 75%
of all cerebral infarctions occur due to middle cerebral
artery occlusion. Occlusion of the posterior inferior
cerebellar artery (PICA) causes infarction of the lateral
medulla plus the inferior cerebellar peduncles
( Wallenberg’s syndrome ).
Imaging strokes involves the assessment of 4 Ps:
Parenchyma : assess the area of stroke and exclude
hemorrhage (Checked by unenhanced CT).
Pipes : assess the extra- and intracerebral blood ves-
sels (carotid and vertebral arteries). Scanning for
CTA should start from the head to the aortic arch.
Perfusion : assess cerebral blood volume (CBV),
cerebral blood fl ow (CBF), and mean transient time
(MTT)
Penumbra : the concept of penumbra in stroke refers
to the salvageable brain tissue. When a vascular
insult occurs, the infracted tissue is surrounded by a
region of stunned tissue due to reduction of the blood
fl ow within the affected region. The identifi cation of
the penumbra helps the decision of using thrombolytics in acute stroke cases. On CT, the penumbra
is assessed by showing parameters mismatch, while
on MR, it is assessed by showing diffusion/perfusion
mismatch. Pneumbra = MTT minus CBV.
Thrombolytics are not given to stroke patients beyond 3
h from starting of the symptoms due to the risk of hemorrhage. Hemorrhage is an absolute contraindication
for thrombolytic therapy. Stroke is evaluated on unenhanced CT, CT-angiography, and CT perfusion study.
Hemorrhagic infarction is usually caused by hypertension or embolic occlusion. Hemorrhagic infarctions
arise due to two mechanisms:
Venous thrombosis : the high fl owing arterial blood is
obstructed by a blocked vein, which raises the intracapillary pressure causing them to rupture and bleed.
Lacunar infarctions ( cerebral microangiopathy ) are
infarctions less than 1 cm in size and occur due to
occlusion of the penetrating arterioles of the brain
parenchyma. Usually, they are seen in the basal ganglia, the thalamus, and the internal capsule. Lacunar
infarctions are commonly seen in diabetic patients.
D i ff erential Diagnoses and Related Diseases
Pusher syndrome: is a very specifi c disease of postural
orientation, commonly affecting poststroke hemiparetic patients. In the pusher syndrome, patients use
their nonparetic arm and/or leg to actively push from
the nonparalyzed side toward the paralyzed, which
results in loss of balance and falling toward the paralyzed side (Fig. 2.1.1 ). These patients also resist any
attempt to correct their tilted body posture toward the
vertical upright position. Pusher syndrome can be seen
in up to 10% of patients with hemiparesis due to
strokes. Pusher syndrome may be also arising due to
brain trauma or tumors.
Signs on CT
Hyperacute stage (the fi rst 3–6 h): unenhanced CT usually is
normal. It must be repeated after this period within 24–48 h.
Acute stage
(from 6 to 24 h): nonenhanced CT shows a
wedge-shaped hypodense area surrounded by edema that
may cause mass eff ect on the ventricles with eff acement of
the cerebral sulci (Fig. 2.1.2a ). The hypodense lesion follows a
vascular territory (Fig. 2.1.3 ). Cytotoxic edema starts after 30
min from the stroke attack, and vasogenic edema starts from
4 to 6 h postattack. Each increase in 1% of parenchymal
edema reduces the Hounsfi eld unit (HU) by 2.5 HU.
Subacut stage (days to weeks): there is a hypodense lesion
without edema (Fig. 2.1.2b ). Edema resolve and the mass
eff ect decrease at 7–10 days postattack.
Chronic stage (more than 3 months postattack): the tissues
around the lesion will loose their volume (gliosis), which will
cause negative pressure upon the adjacent ventricles, causing
2.1 Stroke (Brain Infarction) 43
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their dilatation ( Evacuee Dilatation ) (Fig. 2.1.2c ). When the
evacuee dilatation is massive, the negative pressure causes
the ventricle to open into the infarction, creating a porencephalic cyst (Fig. 2.1.2d ). Porencephalic cyst is a cerebrospinal
fl uid cyst that is communicating with the ventricles.
Hyperdense vessel sign
: on nonenhanced CT, a thrombosed
vessel may appear as a hyperdense structure due to the
thrombus within it. Normal blood measures (40–60 HU) and
is normally not seen on nonenhanced CT, while thrombosed
blood measures (77–80 HU) and can appear on nonenhanced
CT. The thrombosed blood vessels usually asymmetric,
bilateral symmetrical hyperdense vessel is unlikely to be
thrombosis.
: hypoattenuation and
Obscuration of the lentiform nucleus
obscuration of the lentiform nucleus due to cytotoxic edema is
another sign of acute infarction.
Insular ribbon sign : it refers to hypoattenuation of the insular
region with loss of the gray-white matter defi nition.
HU window alteration : the standard HU window setting is (80
HU widths, and 20 HU center). If no abnormality in
attenuation is seen in the image, lower the window to (8 HU
widths, and 32 HU center). The last settings increase the
sensitivity for detection of hypodense areas.
Luxury perfusion : When you inject contrast into an acute
infarction, you’ll get contrast diff usion as multiple lines into
the gyri (Fig. 2.1.4 ). This sign appears within the fi rst 3 days of
the attack. It is best recalled by Elster’s Rule of 3 (as early as 3
days, maximum at 3 days to 3 weeks and gone by 3 months).
Hemorrhagic infarction is seen as an area of hyperdense blood
within the brain parenchyma surrounded by hypodense area
of cytotoxic edema.
Fig. 2.1.1. An illustration demonstrates pusher syndrome; the
patient is actively pushing and extending his right side (nonparalytic side) toward the left side (paralytic side), which is assisted
by the nurse
Lacunar infarction is seen as a small (<2 cm), hypodense area
within the brain parenchyma with no mass eff ect (Fig. 2.1.5 ).
Disruption of the normal circle of Willis branches is classically
detected in stroke (Fig. 2.1.6 ).
44 Chapter 2 Neurology
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Fig. 2.1.2. Multiple axial
CT of the brain with different
stages of infarction:
( a ) acute infarction, ( b )
subacute infarction, ( c )
chronic infarction with
2.1
gliosis, ( d ) chronic infarction
with formation of porencephalic cyst ( arrowhead )
Fig. 2.1.3. Sequential axial
brain MR-illustrations
demonstrates different
vascular territories of the
brain parenchyma
2.1 Stroke (Brain Infarction) 45
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Fig. 2.1.4. Axial brain CT illustration demonstrates infarction
within the vascular region of the middle cerebral artery with
multiple enhanced lines inside it representing luxury perfusion
Fig. 2.1.6. Axial brain CTA image of a patient with left brain
infarction shows blockage of the left middle cerebral artery
(M1) segment ( arrowhead )
Signs on MRI and DWI
Hyperattenuated vessel sign : it is seen on T2* images as
hyperintense vessel (like on unenhanced CT images).
T2* images : are very sensitive to detect hemorrhage and
microhemorrhages. Hemorrhage is seen as areas of abnormal
blooming, while hemosiderin is seen as areas of low signal
intensities.
: areas of infarction are seen as areas of high signal
DW I
intensity due to water motion impedance (cytotoxic edema),
usually 30 min from the start of the attack (Fig. 2.1.7 ). On the
ADC map, the areas of high signal intensity on DWI show low
signal intensity. Chronic infarction shows low signal intensity
on DWI, and high signal intensity on ACD maps. The two must
be assessed together to diagnose chronic infarction. DWI is
accurate in detecting brain stem and lacunar infarctions.
MR Spectroscopy in infarction shows high lactate, and low
N -acetyl aspartate, cholin, and creatine (present up to 5
weeks postattack).
Fig. 2.1.5. Axial brain CT image shows acute lacunar infarction
in the right centrum semiovale with small ring of cytotoxic
edema around it ( arrowhead )
46 Chapter 2 Neurology
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2.1
Fig. 2.1.7. Axial brain DWI shows acute lacunar infarction in
the left paraventricular area ( arrowhead )
For Further Reading
1 . Srinivasan A et al State-of-the-art imaging of acute stroke.
RadioGraph. 2006;26:S75–95
2 . Vu D et al Non-contrast CT in acute stroke. Semin
Ultrasound CT MRI. 2005;26:380–6
3 . Mullins ME. The hyperdense cerebral artery sign on CT
scan. Semin Ultrasound CT MRI 2005;26:394–403
4 . Shetty SK et al CT perfusion in acute stroke. Neuroimaging
Clin N Am. 2005;15:481–501
5 . de Lucas EM et al CT protocol for acute stroke: tips and
tricks for general radiologists. RadioGraph. 2008;28:
1673–87
6 . Karnath H-O. Pusher syndrome – a frequent but little-
known disturbance of body orientation reception. J Neurol.
2007; 254:414–24
7 . Johannsen L et al “Pusher syndrome” following cortical
lesions that spare the thalamus. J Neurol. 2006;253:455–63
2.2 Stroke Diseases and Syndromes 47
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2.2
Stroke Diseases and Syndromes
Stroke can be a symptom rather than an actual disease.
Some systemic diseases present in the form of stroke.
Other diseases or syndromes are associated with stroke
as one of their diagnostic criteria. Some syndromes or
diseases arise due to stroke in a certain area of the
brain. This topic discusses some of the known and
uncommon causes, syndromes, and diseases of stroke.
Moyamoya Disease
(Progressive Occlusive Arteritis)
Moyamoya disease is characterized by a progressive
occlusion of arteries of the circle of Willis due to intimal wall thickening of the distal internal carotid artery
and its proximal anterior cerebral artery branch bilaterally, with the formation of abnormal collateral networks that develop adjacent to the stenotic vessel.
These collaterals give the shape of puff of smoke,
which is called “Moyamoya” in Japanese.
Moyamoya disease is a rare disease worldwide, but
with high incidence in Japanese. Occlusion usually
occurs in both hemispheres, but unilateral occlusion
can occur. The disease can be seen in association with
sickle cells disease and neurofi bromatosis.
The disease peaks in the fi rst decade and dips in the
fourth decade. Patients present in young age with
recurrent strokes, headaches, and behavioral disturbance. The disease can be suspected in a young adult
presenting with stroke, with no predisposing factors.
Diagnosis is essentially established by angiography or
MR-angiography.
Signs on CT, MRI, and MR-Angiography
Large network of collaterals in the basal ganglia and brain
stem fed by the internal carotid artery, the basilar artery, and
the anterior cerebral artery giving the appearance of a puff of
smoke (Pathognomonic) (Fig. 2.2.1 ).
On T1W images, there are multiple hypointense, fl ow void
lesions located in the basal ganglia representing the abnormal
collaterals networks (Fig. 2.2.2 ).
Fig 2.2.1. MR-angiography of a
patient with moyamoya disease
( a ) and MR-angiography in a
normal healthy patient ( b ) for
com parison. In ( a ), there is
irregular arterial collateral
formation in the region of the
anterior cerebral arteries
bilaterally in fi gure ( a )
( arrowheads ), with complete
disappearance of the middle
cerebral artery (MCA) (M1
segment). Compare the image
in ( a ) with the normal MRI
appearance of the circle of
Willis in ( b )
48 Chapter 2 Neurology
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Fig. 2.2.2. Axial T1W brain
MR-illustration ( a ) with axial
FLAIR MRI of a patient with
moyamoya disease shows
multiple fl ow void signal
intensities in the region of the
2.2
basal ganglia bilaterally
representing the abnormal
collateral formation
( arrowheads ). Leuko-
encephalopathy at the region
of the posterior horns of the
lateral ventricles can be seen
( arrow ) affecting the right
side more than the left side
Cerebral Amyloid Angiopathy
Cerebral amyloid angiopathy (CAA) is a disease that
occurs due to deposition of a protein (AB peptide) or
amyloid substance in the arteriolar wall of the cerebral
vessels, causing weakening and fragility of blood vessel walls. Later, intracerebral bleeding develops due to
spontaneous blood vessels rupture.
In CAA, amyloid proteins replace the contractile
element of the arteriolar muscle layer, leading to
increased fragility of the walls. CAA is not a part of
systemic amyloidosis, and it is the most common cause
of spontaneous, nontraumatic intracranial bleeding in
nonhypertensive elderly patients.
CAA should be suspected when an elderly patient
(60 years) presents with unexplained spontaneous
intracranial bleeding that is lobar and located very
superfi cial in the cortex. It is responsible for up to 20%
of nontraumatic brain hemorrhage and hemorrhagic
infarction, and up to 30% of lobar bleeding.
CAA can be associated with Alzheimer’s disease,
with dementia occuring in up to 40% of cases.
Dementia in CAA patients occurs and progresses much
faster than dementia in patients with Alzheimer’s disease. Diagnosis of CAA is usually done by clinical history and the radiological features of the CT or the
MRI.
Fig. 2.2.3. Axial T1W brain MR-illustration demonstrates cerebral amyloid angiopathy (CAA). There is corticomedullary
bleeding in the left parieto-occipital area surrounded by cytotoxic edema ( arrowhead ). Multiple areas of hypointense signal
intensities scattered within the white matter representing chronic
micro-hemorrhages. An area of low signal intensity is seen in
the right parieto-occipital area representing gliosis ( arrow )
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