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1.8 · Diarrhea and Malabsorption
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1
enter the colon. In the colon, bile salts stimulate water
and chloride secretion, resulting in osmotic diarrhea.
Short bowel syndrome is a term used to describe
symptoms related to dysfunctional terminal ileum (e.g.,
bloating , diarrhea , fecal urgency , fecal incontinence ), with
loss of bile salts in the colon.
5 . Infectious diarrhea : infectious causes like bacteria
( Salmonella , E. coli , Shigella ), viruses ( Rotavirus ), and
parasites ( E. histolytica , Giardia , Cryptosporidium ) all
cause diarrhea by releasing enterotoxins, which causes
in ammatory reaction releasing histamine, nitric oxide,
and serotonin. e diarrhea in infection is a mixture
between osmotic ( due to villi destruction ) and secretory
( due to raised cAMP ).
6 . Endocrine diarrhea : many endocrine disorders cause
diarrhea by secreting neurotransmitters such as VIP,
serotonin, acetylcholine, substance P, and calcitonin, all
of which cause secretory diarrhea. Also, some tumors
cause diarrhea via secretion of the same
neurotransmitters and hormones, for example, carcinoid
tumors ( serotonin ), pancreatic neuroendocrine tumors
( VIP , gastrine ), and medullary thyroid carcinoma
( calcitonin ) .
Sprue
Sprue is a term used to describe diseases characterized pathologically by attening, broadening, and coalescence of villi
and sometimes complete loss of villi. Moreover, the lamina
propria is in ltrated with lymphocytes, plasma cells, and
eosinophils.
Sprue can be divided into tropical sprue and nontropical
sprue, also known as celiac disease. Tropical sprue is a geo-
graphically localized form of malabsorption ( in some tropical
areas ) that is characterized by folic acid de ciency; the disease responses dramatically to folic acid or antibiotics therapy. Celiac dis ease , on the other hand, is a disease characterized
by autoimmune reaction that causes villi destruction a er
ingesting food that contains “gluten,” like wheat, rye, oats, and
barley.
Patients with sprue, like other malabsorption syndromes,
present with steatorrhea, weight loss, and abdominal distension. e mucosal abnormalities in sprue tend to be more
marked in the jejunum than in the ileum. Patients respond
well to gluten-free diet. Celiac disease is seen in patients with
type 1 diabetes mellitus, Down’s syndrome, primary biliary
cirrhosis, Sjögren’s syndrome, and dermatitis herpetiformis
(100 %).
Ulcerative jejunoileitis is an uncommon complication of
celiac disease characterized by multiple benign ulcers of variable depth that is found predominantly in the jejunum, occasionally in the ileum, and rarely in the colon. Patients o en
present with fever, weight loss, abdominal pain, anorexia,
and diarrhea.
Serological test to detect celiac disease includes detection
of serum gliadin IgA antibodies (95 % sensitive) and endo-
mysial antibodies (95 % sensitive and speci c). e gold standard test for diagnosis of celiac disease is jejunal biopsy.
Q: What Are the Main Diff erences Between Celiac
z
Disease and Tropical Sprue?
1. Tropical sprue is associated with folic acid de ciency,
while celiac disease is associated with gluten-rich diet.
2. Tropical sprue patients respond well to folic acid and
antibiotic therapy, while celiac disease patients respond
well to gluten-free diet.
3. Both have the same radiological and histological features,
so history and clinical background of the patient’s recent
travels are essential in di erentiating the two conditions.
Signs on US
1. The signs more frequently recorded in celiac disease
include fl uid-distended small bowel loops, thickened
valvulae conniventes, and increased small bowel
peristalsis; this picture is the equivalent of the
well-described reversed jejunoileal fold pattern .
2. There is increased caliber of the superior mesenteric
artery in patients with celiac disease ranging from 8
to 11 mm, 2–3 cm distal to the artery origin.
Signs on Barium Follow-Through
1 . Dilatation : there is signifi cant dilatation of the small
bowel loops, usually in the mid- and distal jejunum
( constant fi nding in sprue ).
2 . Segmentation : this term applies to moderately large
masses of separated barium associated with dilated
bowel loops. Stringlike strands of barium may be
found between the masses representing barium in
collapsed bowel loops. Segmentation is best seen in
the ileum in advanced cases.
3 . Hypersecretion : this refers to large amount of fl uids
secreted into the intestinal lumen and causes barium
dilution, which is seen as barium fl occulation ( mostly
a constant fi nding in sprue ).
4 . Transient time abnormalities : transient time is the
time required for the barium to traverse the small
intestine and enter the cecum ( average 3 h in adults ).
In sprue, the transient time is prolonged (3–5 h) or
shortened (<30 min) depending on the disease
activity.
5 . Moulage phenomenon : it is a term used to describe
the radiographic appearance of an intestinal lumen
with complete destruction of the intestinal folds. The
barium-fi lled lumen resembles a tube into which
“wax” has been poured and allowed to harden.
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Chapter 1 · Gastroenterology
1
Signs on Abdominal CT
1. There may be intussusception , which is detected on
axial view as “target sign” with crescent hypodense
area inside it representing the mesentery. Enhancing
mesenteric vessels within the mass is frequently seen
(very characteristic).
2 . Ulcerative jejunoileitis is an uncommon complication
where patients present clinically with abdominal
pain, weight loss, fever, and anorexia. There is
thickening and ulceration of the jejunal and ileal
mucosa.
3 . Cavitating lymph node syndrome is a rare severe
complication of celiac disease characterized clinically
by weight loss, anorexia, and diarrhea. Mortality rate
is up to 50 % due to sepsis. There is
lymphadenopathy (2–7 cm in diameter) with
characteristic fat–fl uid level. Diff erential diagnosis
includes lymphoma and bacterial infection
(
. Fig. 1.8.1 ).
4 . Malignancy is detected on CT as a focal bowel wall
thickening with lumen narrowing. Malignancies
associated with celiac disease include lymphoma,
adenocarcinoma, and squamous cell carcinoma.
. Fig. 1.8.2 Axial brain CT illustration that demonstrates the
rare sign of occipital calcifi cation seen in neuro-celiac disease
. Fig. 1.8.1 Axial abdomen CT illustration that demonstrates
the cavitating lymph nodes seen in celiac disease, most
commonly aff ecting the retroperitoneal and the mesenteric
lymph nodes
Signs on Neurological CT
Celiac disease patients may experience attacks of
seizures (1.2–5 % of cases). When neurological
manifestations of celiac disease appear, there are
commonly bilateral cortico-subcortical occipital
calcifi cations without contrast enhancement or brain
atrophy (
. Fig. 1.8.2 ).
k Signs of Celiac Disease on MR Enteroclysis
1 . Fold pattern abnormalities : the valvulae conniventes can
appear normal ( most common ), squared end ( rather than
normal round shaped ), reversed jejunal folds ( decreased
folds in jejunum and increased in ileum ), and moulage sign
( the absence of valvulae due to total atrophy ).
2 . I n reversed jejunal pattern , jejunal folds are decreased if
the number of folds <3-folds per inch, and ileal folds are
increased if the number of folds >5 per inch.
3. Bowel wall thickening (>4mm) is a common ning.
4. Mesenteric lymphadenopathy is found in 45 % of cases.
When the lymphadenopathy is associated with
thickening of bowel wall segments, lymphoma should be
suspected ( the commonest malignancy in celiac disease ).
5 . I n ulcerative jejunoileitis , there is a circumferential
thickening of bowel wall with a bilaminar con guration,
bowel wall deep ulcers, and mucosal hyper-enhancement
( characteristic in patients with celiac disease ) .
Whipple’s Disease (Intestinal Lipodystrophy)
Whipple’s disease (WD) is a rare, multisystemic, infectious
disease characterized by destruction of the intestinal villi and
the lamina propria by macrophages that stain positive with
periodic acid of Schi (PAS) stain due to engulfed glycoprotein material.
1.8 · Diarrhea and Malabsorption
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WD is caused by slow-growing, intracellular, gram-
positive bacterium called Tropheryma whipplei . Humans are
the only known host for this infection. Diagnosis is con rmed by detecting these PAS stain-positive macrophages
a er intestinal biopsy.
Patients with WD clinically complain of steatorrhea, weight
loss, abdominal distension and tenderness, skin pigmentation, lymphadenopathy (usually mesenteric), and intermittent, nondeforming, migratory arthritis (80 % of cases).
Other manifestations include the eye, heart, and nervous system abnormalities. Neurological manifestations of WD
Signs on MRI
On brain T2W and FLAIR images, there may be areas of
hyperintensities aff ecting both temporomesial regions,
include supranuclear gaze palsy, cognitive changes, ataxia,
dementia, and seizures.
Signs on Barium Follow-Through
Unlike sprue, WD usually shows minimal signs of
segmentation and dilatation in comparison to sprue.
However, there is marked thickening of the mucosal
folds, with maybe slightly nodular pattern on barium
fi lms ( most prominent radiological fi nding in WD ).
basal ganglia, thalami, internal capsule, the quadrigeminal
plate, and around the third ventricle seen in patients with
neuro-Whipple disease (
. Fig. 1.8.3 ).
. Fig. 1.8.3 Axial brain T2W MR illustration that demonstrates the MR fi ndings in patients with
neuro-Whipple disease
VIPoma (Werner–Morris Syndrome/
Pancreatic Cholera)
Vasoactive intestinal peptide-secreting tumor (VIPoma) is a
disease characterized by W atery D iarrhea, H ypokalemia,
and low or absence of gastric acid secretion or A chlorhydria
(sometimes referred to also as WDHA syndrome ), as classi-
cally de ned in the medical literature.
Vasoactive intestinal peptide (VIP) induces smooth muscle relaxation of the gastrointestinal tract, stimulating water
secretion into pancreatic juices and bile, inhibits gastric acid
secretion, and inhibits absorption from the intestine. VIPoma
may occur as part of multiple endocrine neoplasia type 1
(MEN 1) or may coexist with bronchogenic carcinoma.
Patients with VIPoma are usually 40 years old typically
presenting with massive watery diarrhea with fecal uid
losses amounting to more than 10 l per day in some
reported cases. e diarrhea has ranged from a few months
to up to 15 years. Other features include weight loss,
abdominal pain, nausea, and vomiting. Hypokalemia manifests during attack resulting in lethargy and marked muscular weakness.
Typically, most investigations are normal including upper
GI endoscopy, barium enema studies, enteroclysis, stool culture for parasitic ova, and urinary 5-HIAA.Urinary levels of
5-hydroxyindole acetic acid (5-HIAA) are used to detect carcinoid tumors of the enterochroma n cells of the small
intestine. 5-HIAA determines the body’s levels of serotonin.
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Chapter 1 · Gastroenterology
Patients with renal failure may show falsely low levels of
1
5-HIAA.Serum potassium levels are usually low during the
diarrheal attacks. Impaired glucose tolerance test has been
observed in several patients with VIPoma and was attributed
to a secondary e ect of chronic hypokalemia. Hypercalcemia
and acidosis are other laboratory features in VIPoma.
Selected Readings
Binder HJ. Causes of chronic diarrhea. N Engl J Med.
2006;355(3):236–9.
Buckle MJ, etal. Neurologically presenting Whipple disease:
case report and review of the literature. J Clin Pathol.
2008;61:1140–1.
Buckley O, etal. e imaging of coeliac disease and its com-
plications. Eur J Radiol. 2008;65:483–90.
Castiglione F, etal. Bowel sonography in adult celiac disease:
Signs on CT and MRI
1. Up to 50 % of VIPoma have distant metastases at the
time of presentation, usually to the liver and lungs.
2. The tumor is detected in the body or the tail of
pancreas (75 %) or in the head of the pancreas (25 %
of cases). On MRI, the tumor is detected with an
intermediate signal on T1W images and high signal
intensity on T2W images. Enhancement may be seen.
Liver metastases are commonly detected (50 % of
cases), which can assist in the diagnosis of VIPoma,
taking into consideration the history, clinical
presentation, and laboratory investigation of the
patient.
diagnostic accuracy and ultrasonographic features.
Abdom Imaging. 2007;32:73–7.
Gobbi G. Coeliac disease, epilepsy and cerebral calci ca-
tions. Brain Dev. 2005;27:189–200.
Kaiser L, et al. Infectious causes of chronic diarrhea. Best
Pract Res Clin Gastroenterol. 2012;26(5):563–71.
Kunzelmann K, etal. Electrolyte transport in the mammalian
colon: mechanisms and implications for disease. Physiol
Rev. 2002;82(1):245–89.
Marshak RH, et al. Malabsorption syndrome. Semin
Roentgenol. 1966;1(2):138–77.
Moser PP, etal. CT ndings of increased splanchnic circula-
tion in a case of celiac sprue. Abdom Imaging. 2004;29:
15–7.
Puget M, et al. Whipple’s disease with muscle impairment.
Muscle Nerve. 2006;34:794–8.
S o a CM, et al. MR imaging of metastatic pancreatic
VIPoma. Magn Reson Imaging. 1997;15(10):1205–8.
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Neurology
2.1 Stroke (Brain Infarction) – 62
Diff erential Diagnoses and Related Diseases – 62
2.2 Stroke Diseases and Syndromes – 66
Moyamoya Disease (Progressive Occlusive Arteritis) – 66
Cerebral Amyloid Angiopathy – 68
CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts
and Leukodystrophy) – 69
MELAS (Mitochondrial Myopathy, Encephalopathy, Lactic Acidosis, and StrokeLike Episodes) – 70
Cortical Laminar Necrosis – 71
Man-in-the-Barrel Syndrome – 72
Locked-In Syndrome – 73
Brain Stem Infarction Syndromes – 73
Subclavian Steal Syndrome – 75
2
2.3 Intracranial Hemorrhage – 76
Epidural Hematoma – 77
Subdural Hematoma – 78
Subarachnoid Hemorrhage – 79
Intracerebral/Intraparenchymal Hemorrhage – 80
Intraventricular Hemorrhage – 81
Hemorrhage into Malignancy – 82
2.4 Meningitis – 82
Diff erential Diagnoses and Related Diseases – 84
2.5 Encephalitis – 85
Limbic Encephalitis – 85
Acute Demyelinating Encephalomyelitis (ADEM) – 87
Hashimoto’s Encephalitis – 88
Rasmussen Encephalitis (Rasmussen Syndrome) – 89
Measles Encephalitis – 89
Subacute Sclerosing Panencephalitis (SSPE) – 90
Japanese Encephalitis – 90
West Nile Encephalitis – 90
Tick-Borne Encephalitis (Spring–Summer Encephalitis) – 90
Murray Valley Encephalitis – 91
St. Louis Encephalitis – 91
Encephalitis Lethargica – 91
© Springer International Publishing Switzerland 2017
J.A. Al-Tubaikh, Internal Medicine, DOI 10.1007/978-3-319-39747-4_2
2.6 Epilepsy – 92
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Diff erential Diagnoses and Related Diseases – 93
2.7 Headache – 96
Migraine – 96
Spontaneous Intracranial Hypotension (Schaltenbrand Syndrome) – 97
Idiopathic Intracranial Hypertension (Pseudotumor Cerebri) – 97
Temporal (Giant) Cell Arteritis – 98
2.8 Multiple Sclerosis and Other Demyelinating Diseases – 99
Multiple Sclerosis – 99
Neuromyelitis Optica (Devic’s Syndrome) – 101
Marburg’s Type MS – 102
Baló Concentric Sclerosis – 103
Schilder’s Disease (Diff use Myelinoclastic Sclerosis) – 103
Susac’s Syndrome – 103
Guillain–Barré Syndrome – 104
2.9 Parkinsonism – 106
Diff erential Diagnoses and Related Diseases – 107
2.10 Dementia – 108
Alzheimer’s Disease – 108
Vascular Dementia – 109
Frontotemporal Lobar Degeneration (Pick’s Disease) – 109
Dementia with Lewy Bodies – 111
Progressive Supranuclear Palsy (Steele–Richardson–Olszewski
Syndrome) – 112
Multiple System Atrophy (Shy–Drager Syndrome) – 112
Subcortical Arteriosclerotic Encephalopathy (Binswanger’s Disease) – 113
Prion Disease – 114
2.11 Huntington’s Disease – 116
Diff erential Diagnoses and Related Diseases – 117
2.12 Heat Stroke (Pancerebellar Syndrome) – 117
2.13 Aphasia – 117
Neural Control of Speech – 118
Aphasia Pathophysiology and Subtypes – 118
2.14 Squint (Strabismus) – 122
Neural Control of Ocular Muscles – 122
Pathophysiology – 122
Related Disorders – 122
2.15 Nystagmus – 124
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Neural Control of Eye Movement – 124
Nystagmus Subtypes – 125
2.16 Erectile Dysfunction – 126
Neural Control Human Sexual Behavior – 126
Pathophysiology – 127
Erectile Dysfunction Diff erential Diagnoses – 127
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Chapter 2 · Neurology
2.1 Stroke (Brain Infarction)
Stroke means the death of brain cells (infarction) due to isch-
2
emia or emboli.
e most common causes of stroke are atherosclerosis,
embolic vascular occlusion, hypertension, and in ammatory
vascular diseases (vasculitis). Patients present with sudden
neurological de cits in the body according to the area of the
brain a ected. 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 ).
D i ff erential Diagnoses and Related Diseases
Pusher syndrome is a very speci c disease of postural orientation, commonly a ecting 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 ). ese 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.
5 Imaging strokes involves the assessment of four Ps:
5 Parenchyma : assess the area of stroke and excludes
hemorrhage (checked by unenhanced CT).
5 Pipes : assess the extra- and intracerebral blood vessels
(carotid and vertebral arteries). Scanning for CTA should
start from the head to the aortic arch.
5 Perfusion : assess cerebral blood volume (CBV), cerebral
blood ow (CBF), and mean transit time (MTT).
5 Penumbra : the concept of penumbra in stroke refers to the
salvageable brain tissue. When a vascular insult occurs, the
infarcted tissue is surrounded by a region of stunned tissue
due to reduction of the blood ow within the a ected
region. e identi 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 di usion/
perfusion mismatch. Penumbra = MTT minus CBV.
rombolytics are not given to stroke patients beyond 3h
from the start 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:
5 Venous thrombosis : the high owing arterial blood is
obstructed by a blocked vein, which raises the
intracapillary pressure causing them to rupture and bleed.
5 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.
Lacunar infarctions ( cerebral microangiopathy ) are infarc-
tions less than 1cm 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.
. 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
2.1 · Stroke (Brain Infarction)
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2
Signs on CT
5 Hyperacute stage (the fi rst 3–6 h): unenhanced CT
usually is normal. It must be repeated after this period
within 24–48 h.
a
5 Acute stage (from 6 to 24 h): nonenhanced CT shows a
wedge-shaped hypodense area surrounded by
edema that may cause mass effect on the ventricles
with effacement of the cerebral sulci (. Fig. 2.1.2a ).
b
c
. Fig. 2.1.2 Multiple axial CT of the brain with diff erent stages of infarction: ( a ) acute infarction, ( b ) subacute infarction, ( c ) chronic
infarction with gliosis, and ( d ) chronic infarction with formation of porencephalic cyst ( arrowhead )
d
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Chapter 2 · Neurology
The hypodense lesion follows a vascular territory
(. Fig. 2.1.3 ). Cytotoxic edema starts after 30 min
2
from the stroke attack, and vasogenic edema starts
from 4 to 6 h postattack. Each increase in 1 % of
parenchymal edema reduces the Hounsfield unit (HU)
by 2.5 HU.
5 Subacute stage (days to weeks): there is a hypodense
lesion without edema (. Fig. 2.1.2b ). Edema resolves
and the mass effect decreases at 7–10 days
postattack.
5 Chronic stage (more than 3 months postattack): the
tissues around the lesion will lose their volume
(gliosis), which will cause negative pressure upon the
adjacent ventricles, causing 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.
5 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 are usually
asymmetric, and bilateral symmetrical hyperdense
vessel is unlikely to be thrombosis.
5 Obscuration of the lentiform nucleus : hypoattenuation
and obscuration of the lentiform nucleus due to
cytotoxic edema are another signs of acute infarction.
5 Insular ribbon sign : it refers to hypoattenuation of the
insular region with loss of the gray–white matter
definition.
5 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).
5 Hemorrhagic infarction is seen as an area of
hyperdense blood within the brain parenchyma
surrounded by hypodense area of cytotoxic edema.
5 Lacunar infarction is seen as a small (<2 cm),
hypodense area within the brain parenchyma with no
mass effect (. Fig. 2.1.5 ).
5 Disruption of the normal circle of Willis branches is
classically detected in stroke (. Fig. 2.1.6 ) .
Middle cerebral artery
Anterior cerebral artery
Posterior cerebral artery
. Fig. 2.1.3 Sequential axial brain MR illustrations demonstrate diff erent vascular territories of the brain parenchyma
Recurrent artery of Habenur
Lenticulo-striate artery
Anterior choroidal artery
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