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Fig. 10.15 Two epileptic patients with hamartomas of the tuber cinereum. The upper row shows a large tumor in the oor of the 3° ventricle
extending into the suprasellar region with a similar signal to the hippocampus on T1 (a, b) and T2 sequences (c, d) (arrows). The patient has
h
a retrocerebellar cyst. The lower row shows a small hamartoma inside
the 3°ventricle with the same signal as the gray matter on sagittal
FLAIR (e), coronal T1MPRAGE (f), and axial and coronal T2 (g and h)
(arrows)
10.5 Other Causes ofFocal Epilepsy
Many other pathologies can cause seizure. Similar to the previous paragraph, it is beyond the scope to in detail describe
imaging features of vascular malformations, infections, or
trauma that can go along with seizures, and most of the entities are described in other chapters of this syllabus. We therefore only want to highlight few epilepsy-relevant facts and
features of these conditions.
Vascular malformations can cause seizures due to previous hemorrhage and scarring, hemosiderin deposition (especially when close to the cortex), or gliosis. AVMs in the
temporal lobe have a higher likelihood of producing seizure
due to interference of the normal blood supply and drainage
of potentially epileptogenic structures such as the
hippocampus.
Cavernous malformations that are cortically located and
have hemosiderin staining reaching the cortex, and in particular the mesial temporal lobe structures, are very often
associated with seizures as the hemosiderin stain is believed
to have a strong irritative potential for neurons. They are best
visualized on T2 gradient echo or SWI sequences where they
demonstrate with the classical blooming artifact (Fig.10.16).
Patients with previous trauma can experience posttraumatic seizure disorder, especially after having sustained
contusional hemorrhages of their temporal lobes as gliosis
and hemosiderin staining can cause irritation of the surrounding cortex.
Neonatal anoxic ischemia or hypoxemia can cause ulegyria—i.e., a scar/defect of the cerebral cortex that mainly
involves the cortex in the depth of the sulcus, whereas the
cortical crowns remain relatively unaffected [24].
If the perinatal ischemia has only involved one hemisphere (perinatal stroke), a Dyke-Davidoff-Masson syndrome will ensue where stable hemiatrophy is present with
hypertrophy of the skull and the sinuses, paucity of white
matter, ventricular enlargement, and mild gliosis (Fig.10.17).
Virtually any infection (bacterial, fungal, parasitic) can
produce epileptogenic lesions, and worldwide infections are
the leading cause of epilepsy (Fig.10.18). A typical example
is neurocysticercosis which is a very common cause of focal
epilepsy in the developing world.
Antero-basal temporal lobe encephaloceles are lesions
that are either related to a congenital defect of the bone or to
previous trauma. Brain tissue can extend into the pterygopalatine fossa through the bony defect at the base of the
greater sphenoid wing in the region of the foramen rotundum
and pterygoid process. The herniated brain demonstrates
high T2/FLAIR signal and is believed to be the epileptogenic
focus (Fig.10.19). Following resection of the abnormal brain
tissue seizure freedom can be obtained in a very large proportion of cases.
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N. Bargalló and T. Krings
Fig. 10.16 Patient with temporal lobe epilepsy, showing a typical cavernoma nding with (a) popcorn appearances on T1 coronal, and surrounded by hemosiderin in the white matter seen on (b) coronal FLAIR,
(c) coronal T1, and (d) axial T2 sequences. Note that the right amygdala
and hippocampus are normal
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Fig. 10.17 A 16-year-old boy with perinatal vascular injury and epilepsy and right hemiparesis. A large porencephalic cyst that involves
the part of the left middle cerebral artery territory. The cyst shows some
septa and contacts with the ependyma of the left lateral ventricle. There
is an abnormal signal in white matter indicating gliosis and Wallerian
degeneration. Note the hypertrophy of the left side of the skull and
asymmetric enlargement of the frontal sinus (a, b) axial T2WI; (c) coronal FLAIR. (d) SISCOM indicates that the seizure onset zone is in the
midsagittal cortex near the porencephalic cyst
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Fig. 10.18 A 35-year-old female with a previous history of meningitis
and epilepsy. MRI (a) axial T2WI (b) coronal FLAIR shows atrophy of
the left temporal lobe with white matter hyperintensity associated with
left HS (arrow). (c) SISCOM images indicate that the ictal onset zone
Rasmussen’s encephalitis is a presumably autoimmunemediated chronic inammation of the brain that presents
with progressive gliosis and volume loss. Patients experience
seizures and a progressive hemiparesis (Fig.10.20).
initiates in the left neocortical temporal lobe. (d) Language fMRI demonstrates activation of the right hemisphere during an auditive comprehension paradigm, indicating that the language function has been
transferred to the other hemisphere
Key Point
• Many other pathologies including vascular malformations, phakomatoses, or remote infections or
trauma can cause medication refractory epilepsy,
particularly if they involve the gray matter.
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Fig. 10.19 Patient with temporal lobe epilepsy. MRI exam (a) T2 coronal and (b) axial T2MRI show the left temporal pole extending into the
pterygopalatine fossa throughout a small defect of the left greater sphenoid wing seen on (c) coronal CT (arrows)
Fig. 10.20 A 9-year-old patient with continuous partial seizures arising from the right hemisphere, progressive cognitive deterioration, and
left hemiparesis. MRI studies over time show progressive atrophy of the
right lentiform and caudate nuclei with progressive right hemisphere
atrophy. (Axial 3DT1 upper row, axial T2 lower row)
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N. Bargalló and T. Krings
10.6 Concluding Remarks
Neuroimaging in patients with medication refractory epilepsy should identify clinically relevant abnormalities in a
high percentage of cases and therefore the radiologist plays a
crucial role in the identication of epileptogenic lesions and
their possible surgical removal. A dedicated epilepsy protocol is necessary to identify these lesions, and the MR should
be interpreted and multidisciplinary rounds with radiological
input are paramount to manage these challenging patients.
Take-Home Messages
• When evaluating a dedicated seizure protocol MR,
a structured approach is helpful that includes a
detailed assessment of (a) the hippocampus and
mesial temporal lobe structures, (b) the ventricular
outline, and (c) the gyral and the sulcal anatomy.
• Particular emphasis should be paid upon the T2/
FLAIR signal within the cortex and hippocampus,
its similarity to other regions of neo- and archicortex, the internal architecture of the hippocampus,
the indentations of the head of the hippocampi, the
fornix and mammillary bodies, and the gray–white
matter interface of the neocortex (blurring, gray
matter thinning, or thickening).
• The malformations of cortical development can be
differentiated into disorders of neuronal proliferation, migration, and cortical organization and can
be diffuse or very subtle. There are slow growing
tumors, usually neuroglial lineage that are associated with chronic epilepsy.
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2. Hauser WA, Beghi E.First seizure denitions and worldwide incidence and mortality. Epilepsia. 2008;49(Suppl 1):8–12.
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21. Severino M, et al. Denitions and classication of malformations of cortical development: practical guidelines. Brain.
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org/licenses/by/4.0/), which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropri-
ate credit to the original author(s) and the source, provide a link to the Creative Commons license and indicate if changes were made.
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Found Down
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Imaging Evaluation of the Patient Found
Unconscious
ChristopherP.Hess andJamesG.Smirniotopoulos
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Keywords
Unconscious · Coma · Emergency · Trauma · Hypoxia
Hydrocephalus · Herniation · Ischemia · Stroke · Seizure
Overdose · Metabolic · Infection
Learning Objectives
• To understand the spectrum of disorders that may
cause a patient to become unconsciousness.
• To appreciate the central role of imaging in the evaluation of patients found unresponsive.
• To recognize key imaging ndings that dene diagnosis, drive treatment, and predict outcome in the
unconscious patient.
Consciousness is believed to arise from two inter-related
brain functional states: wakefulness, reecting an individual’s level of arousal and response to external stimuli, and
awareness, representing the content of one’s conscious experience and the ability to interact with the external environment. Disruption to either or both states may result in a
patient being “found down.” The inability to take an accurate
medical history, the limitations of physical examination in
the obtunded patient, and the need to rapidly make treatment
decisions position imaging centrally within the evaluation of
most of these patients. Radiologists should be prepared to
help decide on an appropriate imaging strategy, suggest a
limited differential diagnosis as to root causes for the
patient’s condition, identify problems that mandate emergent
medical or surgical intervention and, in some cases, assist in
dening short- and long-term prognosis.
Any disruption to the normal brain chemistry, structure,
metabolism, or function may cause a patient to become
unconscious. Because the brain has a remarkable ability
adapt to chronic stress, disorders of arousal usually come as
the result of acute rather than longstanding disease. Acute
trauma (known or occult) and cardiorespiratory failure are
the most frequent causes. In one study of seven major centers, roughly one third of patients found down were initially
triaged for trauma, and two thirds were triaged for medical
illnesses [1]. The majority (74.1%) underwent head CT at
some point during their treatment, typically during initial
assessment but also later during their hospitalization. The
delayed use of imaging derived in part from the fact that
nearly half (47.7%) of patients suffered from comorbid traumatic and medical illness.
Given the frequency of traumatic injury in patients found
down, it is convenient to divide causes for unconsciousness
into traumatic and non-traumatic. In both cases, the brain
may be involved either from a primary insult or from secondary dysfunction due to other systemic disorders such as sepsis, metabolic derangement, toxic exposure, hypotension, or
hypertension (Table11.1). Among primary brain abnormalities, diseases caused by diffuse neuronal dysfunction should
be distinguished from diseases that disproportionately
involve the individual anatomic structures that contribute to
consciousness (Table11.2) [2]. We highlight several important diagnoses with actionable ndings that may be identied in imaging studies of patients who are found down.
C. P. Hess (*)
Department of Radiology and Biomedical Imaging, University of
California, San Francisco, San Francisco, CA, USA
e-mail: christopher.hess@ucsf.edu
J. G. Smirniotopoulos
MedPix® Medical Image Database, National Library of Medicine,
Bethesda, MD, USA
e-mail: james.smirniotopoulos@nih.gov
© The Author(s) 2024
J. Hodler et al. (eds.), Diseases of the Brain, Head and Neck, Spine 2024-2027, IDKD Springer Series,
https://doi.org/10.1007/978-3-031-50675-8_11
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C. P. Hess and J. G. Smirniotopoulos
Table 11.1 General differential considerations in the imaging evaluation of patients found down
Acute traumatic brain injury
Acute vascular abnormalities
Hypoxia and hypoperfusion
Seizures
Elevated or low intracranial pressure
Herniation syndromes
Viral encephalitis
Acute necrotizing encephalopathy
Toxic exposures, for example:
Carbon monoxide
Methanol
Ethylene glycol
Organophosphates
Metabolic abnormalities, for example:
Hypoglycemia and hyperglycemia
Hyponatremia and hypernatremia
Uremia
Hyperammonemia
Wernicke’s encephalopathy
Osmotic demyelination
Table 11.2 Anatomic brain structures contributing to the conscious
state
Brainstem (especially nuclear components of the reticular activating
system)
Hypothalamus (especially midline paraventricular nuclei)
Anterior striatum
Claustrum
Thalamus (especially central nuclei)
11.1 Structural andVascular Abnormalities
Traumatic axonal injury (TAI), a severe form of traumatic
brain injury that often renders patients’ unconscious, represents up to half of all brain injuries after severe trauma in the
United States [3]. High-speed motor vehicle accidents, shake
injuries to infants, fall from heights—any major traumatic
mechanism associated with rapid acceleration-deceleration
of the brain relative to the skull can lead to TAI.Exposed to
mechanical shear, structures within the brain with different
tensile strength, viscosity, and microscopic architecture suffer from stretch or tear injuries of axons, cell bodies and
myelin, disruption of normal chemical processes, and abnormal cellular function. Although all areas of the brain may be
involved, TAI most often affects the corpus callosum, the
brainstem (especially the dorsal midbrain), and cortical graywhite interfaces. Findings are evident on CT only in the most
severe injuries, in which tiny foci of parenchymal hemorrhage are observed. Susceptibility-sensitive and diffusionweighted MRI are usually necessary to detect and characterize
the extent of TAI and show multiple focal areas of signal
abnormality in typical brain areas (Fig.11.1).
After trauma, hypoxic insults from cardiac or respiratory
failure, as may result from cardiac arrest, shock, choking, or
drug overdose, represent the most common cause for diffuse
brain injury in the patient found down. The degree to which
the brain is injured depends upon the severity and duration of
deprivation of oxygen and/or reduced perfusion, which is
required to make glucose that supplies the brain’s energy.
Complete anoxia, even for short periods, usually involves the
entirety of the brain. When oxygen in the blood is insufcient to support energy production, the most metabolically
active areas of the brain are disproportionately affected. The
hippocampus, basal ganglia, thalami, and cerebellum are
most often involved in adults suffering from global hypoxic
and ischemic injuries. Importantly, the imaging appearance
of hypoxia also depends on the timing of imaging relative to
the injury. Swelling and loss of normal gray-white differentiation in the acute phase progresses to atrophy in chronic
stages, and white matter abnormalities are delayed with
respect to those in gray matter. Early evidence of hypoxic
injury on both CT [4] and MRI [5] have been advocated as
useful markers to predict clinical outcome.
Low cerebral perfusion pressure due to systemic hypotension or intracranial hypertension, which occurs together with
hypoxia, may also cause patients to become acutely unconscious (Fig.11.2). In this scenario, it is the border-zone or
“watershed” areas of the brain—in-between vascular territories—that are most impacted. Reduced cerebral blood ow
not only causes cellular ischemia, but also results in platelet
microemboli that lodge preferentially within end arteries,
especially the leptomeningeal arteries that overlie arterial
border zones [6]. The degree of injury may be most severe in
vascular territories that lie distal to pre-existing arterial stenosis, for example, distal to from carotid or intracranial atherosclerosis. Hypoperfusion injury is diagnosed when
wedge-shaped areas of injury are evident between affected
arterial territories or in a linear “string of pearls” pattern paralleling the lateral ventricles.
Although CT can detect watershed injury in the patient
found down, MRI is usually necessary to characterize the
severity and extent of injury. This is especially the situation
for micro-occlusive disease, such as occurs in thrombotic
microangiopathy. Here, low cerebral perfusion pressure
occurs in the microcirculation of the brain because of in situ
occlusions within capillaries, arterioles, and sometimes
venules from cerebral vasculitis, intravascular lymphoma,
disseminated intravascular coagulation, or thrombocytopenia, for example [7]. This diagnosis is particularly challenging to make in the unconscious patient and relies on the MRI
observation of multiple tiny foci of susceptibility signal
change scattered throughout the brain, often together with
edema and punctate foci of reduced diffusion.
Diffuse brain disease can be distinguished from other disorders that directly impact the brain areas that are responsible
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Fig. 11.1 Diffuse brain
injury. (a) Axial T2*weighted gradient echo MRI
shows diffuse axonal injury,
with multiple foci of
susceptibility in a patient
found unconscious after
high-speed motor vehicle. (b)
Axial diffusion-weighted
MRI in a patient after global
hypoxia, with relatively
symmetric involvement of the
basal ganglia. (c) Axial
unenhanced CT 4h following
cardiac arrest, with diffuse
parenchymal swelling and
loss of gray-white
differentiation. (d) Axial
unenhanced CT showing
reversal of normal gray and
white matter density in a
patient 6days after being
found unresponsive
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Fig. 11.2 Hypoperfusion
injury. (a) Axial diffusion
trace MRI showing watershed
injury after acute aortic
dissection, with wedgeshaped infarcts in the
junctional zones of the right
anterior and middle cerebral
arteries and the right middle
and posterior cerebral arteries.
(b) Axial susceptibilitysensitive MRI in a patient
with autoimmune hemolytic
anemia and diffuse
thrombotic microangiopathy,
showing innumerable foci of
intravascular susceptibility
and associated edema
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Fig. 11.3 Localized brain
abnormalities. (a) Axial
unenhanced CT showing
hyperdense basilar artery
from thrombotic occlusion.
(b) Axial unenhanced CT
with internal cerebral venous
thrombosis, seen as
hyperdense internal cerebral
veins with venous edema in
the thalami and basal ganglia.
(c) Axial T2 FLAIR MRI in a
comatose patient with
Japanese encephalitis. (d)
Axial T2-weighted MRI in a
child found unresponsive after
febrile illness, diagnosed with
acute necrotizing
encephalopathy
C. P. Hess and J. G. Smirniotopoulos
for maintaining the brain’s conscious activity (Fig. 11.3).
Insults to the thalamus, hypothalamus and brainstem may
cause patients to become unresponsive. Interruption of the
viral infection, ANE results from delayed immune-mediated
injury to these structures [8]. The disease is more common in
genetically susceptible individuals.
arterial supply or venous drainage of the thalami and brainstem, especially from basilar artery thrombosis or internal
cerebral venous thrombosis, are critical abnormalities to
identify on CT examinations of patients found down. Certain
viral illnesses, such as West Nile virus, Japanese encephalitis, Murray Valley encephalitis, Eastern equine encephalitis,
and inuenza A, also have a predilection for selective
involvement of the thalami and brainstem. Acute necrotizing
encephalopathy (ANE), a para-infectious disorder that follows acute viral illness, is also associated with symmetric
Key Point
• Loss of consciousness may result from any process
that structurally involves the entire brain or specically impacts the brainstem, the hypothalamus, or
the thalamus. MRI is typically more sensitive for
most disorders, especially early following the onset
of hypoxia, hypoperfusion, or ischemia.
abnormalities of the thalami. In contradistinction to direct
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11.2 Intracranial Pressure andHerniation
Syndromes
Intracranial pressure (ICP) normally ranges from 7 to 15mm
Hg in supine adults and increases or decreases in response to
changes in volume of the structures contained within the
rigid skull—brain, blood, and cerebrospinal uid (CSF). ICP
is distributed relatively equally within the cranium, including
the intra- and extra-ventricular CSF spaces and across the
different intracranial compartments dened by bony boundaries and by the rigid falx and tentorium cerebelli. Patients
may lose consciousness because of abnormally increased or
decreased ICP, when the pressure gradients across intracranial compartments give rise to herniation and brain compression syndromes, and when elevated intraventricular pressure
causes hydrocephalus. In each scenario, the mechanical distortion of the brain and/or associated reduction in its normal
Fig. 11.4 Brain swelling and
herniation. (a) Axial
unenhanced CT showing
diffuse brain swelling in the
setting of severe
hyponatremia, with diffuse
effacement of sulci and
ventricular compression. (b)
Axial unenhanced CT
showing right
holohemispheric subdural
hematoma with leftward
midline herniation in an
elderly patient on
anticoagulants. (c) Midline
sagittal T2 FLAIR MRI
showing ndings of
intracranial hypotension. (d)
Axial unenhanced CT with
hydrocephalus due to third
ventricular colloid cyst
a
perfusion disrupts brain function, causing the patient to fall
unconscious.
Diffuse brain swelling, space-occupying lesions, and
hydrocephalus all cause elevated ICP.Hypertension, metabolic derangements, hypoxia, ischemia, meningitis, traumatic injury, and other disorders may be sources of
life-threating diffuse swelling (Fig. 11.4). Although mild
swelling can be difcult to recognize on imaging studies,
more severe swelling is associated with signicant narrowing of convexity sulci, ventricular compression, and effacement of the normal CSF cisternal spaces (e.g.,
peri-mesencephalic and suprasellar cisterns). Its diagnosis
relies on the observation of diffusely diminished CSF spaces,
venous dural sinus narrowing, and attening of the posterior
sclera, enlargement and tortuosity of the optic nerve sheath,
and protrusion of the optic papilla (an imaging correlate to
papilledema) [9]. Intracranial hemorrhage and tumors of a
b
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