high magnetic field, they are not compatible
with certain types of implants in patients, in-
cluding cardiac pacemakers and deep brain
stimulators. Patients who require mechanical
ventilation must either be ventilated by hand
during the scan or placed on a specialized
MR-compatible ventilator. In addition, most se-
quences take substantially longer than CT scans,
so that clear images require that the patient not
move.
MRA can reveal most stenoses or occlusions
of cerebral blood vessels. It requires only a few
additional minutes during a conventional MRI
scanning session, and the images are extracted
by computer and therefore can be recovered
very quickly. However, the MRA is very flow
dependent, and tends to exaggerate the degree
of stenosis in areas of slow flow.
Magnetic Resonance Spectroscopy
Magnetic resonance spectroscopy (MRS)
156
is
becoming increasingly important in the diag-
nosis and prognosis of patients with a variety of
illnesses that cause delirium, stupor, or coma
(Figure 5–7). The technique identifies neuro-
chemicals in regions of both normal and ab-
normal brain. Although special techniques al-
low the identification of as many as 80 brain
metabolites, most clinical centers using stan-
dard MRI machines perform proton (
1
H) MRS
Figure 2–11. A series of computed tomography (CT) scans through the brain of a patient with a left internal carotid
occlusion. Note that in the noncontrast CT scan in panel (A), there is loss of the gray-white differentiation and effacement
of the sulci over the middle cerebral artery distribution on the left. Panel (B) shows the perfusion blood flow map,
indicating that there is very low flow within the left middle cerebral artery distribution, but that there is also impairment of
blood flow in both anterior cerebral arteries, consistent with loss of the contribution from the left internal carotid artery.
Although the blood volume (C) is relatively normal in these areas, mean transit time (D) is also abnormal, indicating that
tissue in the anterior cerebral distributions is at risk of infarction.
Examination of the Comatose Patient
79
that can identify about 13 brain metabolites
(see Figure 5–7, page 226).
Myo-inositol (mI) is a sugar-like molecule
present in astrocytes. It helps to regulate cell
volume. Its presence serves as a marker of as-
trocytes. The metabolite is elevated in a number
of disorders including hyperosmolar states, pro-
gressive multifocal leukoencephalopathy, renal
failure, and diabetes. Levels are decreased in
hyponatremia, chronic hepatic encephalopathy,
tumor, and stroke.
Creatine (Cr) is actually the sum of creatine
and phosphocreatine, a reliable marker of en-
ergy metabolism in both neurons and astro-
cytes. The total creatine peak remains constant,
allowing other peaks to be calculated as ratios
to the height of the creatine peak.
N-Acetylaspartate (NAA) is an amino acid
derivative synthesized in neurons and trans-
ported down axons. It marks the presence of
viable neurons, axons, and dendrites. Its levels
may be increased in hyperosmolar states and
are decreased in almost any disease that causes
destruction of neurons or their processes.
The choline (Cho) peak represents several
membrane components, primarily phospho-
choline and glycerophosphocholine. Choline is
found in higher concentration in glial cells and
is thus higher in white matter than gray matter.
It is increased in tumors (particularly relative
to NAA), strokes, and hyperosmolar states. It is
decreased in liver disease and hyponatremia.
Glutamate/glutamine (Glx) represents a mix-
ture of amino acids and amines involved in
excitatory and inhibitory transmission as well
as products of the Krebs cycle and mitochon-
drial redox systems. The peak is elevated in
hypoxic encephalopathy and in hyperosmolar
states; it is diminished in hyponatremia.
Lactate (Lac), not visible in normal brain, is
a product of anaerobic glycolysis and is thus
increased in hypoxic/ischemic encephalopa-
thy, diabetic acidosis, stroke, and recovery from
cardiac arrest. It is also increased in highly ag-
gressive tumors.
A lipid peak is not present in normal brain
but is identified in areas of brain necrosis,
particularly in rapidly growing tumors. Cere-
bral fat embolism (see Chapter 5) can also
cause a lipid peak.
157
The clinical use of some of these spectra in
stuporous or comatose patients is discussed in
Chapter 5.
Neurosonography
Intracranial Doppler sonography identifies
flow of blood in arteries, particularly the mid-
dle cerebral artery. The absence of flow in the
brain has been used to confirm brain death,
particularly in patients who have received sed-
ative drugs that may alter some of the clini-
cal findings (see Chapter 8).
158,159
The tech-
nique is also useful for following patients with
strokes, head injuries, and hypoxic/ischemic
encephalopathy.
160,161
The injection of gas-
filled microbubbles enhances the sonographic
echo and provides better delineation of blood
flow, occlusions, pseudo-occlusions, stenosis,
and collateral circulation.
162
Doppler studies of the extracranial carotid
circulation are frequently done as a routine
part of stroke evaluation at many centers. How-
ever, this is rarely helpful for patients in coma.
If the coma is due to a reversible stenosis or
occlusion of a single vessel, it almost always
will be in the vertebrobasilar, not the carotid,
circulation. If the patient is going to receive
an MRI scan, the MRA of the cervical ves-
sels, which examines both the carotid and the
vertebrobasilar circulation, is generally more
revealing.
Lumbar Puncture
Although often overlooked in the technologic
era, the examination of the CSF still plays a
central role in neurologic diagnosis, particu-
larly in patients with a depressed level of con-
sciousness. Once an imaging study has been
performed, it is necessary to proceed with lum-
bar puncture as soon as possible for patients
with no clear diagnosis. Rare patients in whom
subarachnoid hemorrhage was not detected
on imaging may demonstrate blood in the
CSF. Similarly, occasional patients with bac-
terial meningitis or viral encephalitis may pres-
ent with a depressed level of consciousness
(sometimes after a missed seizure), and may
not yet have sufficient meningismus to make
the diagnosis of meningitis clear from exami-
nation. This may be particularly difficult to
determine in patients who have underlying ri-
gidity of the cervical spine (evidenced by re-
sistance to lateral as well as flexion movements
80
Plum and Posner’s Diagnosis of Stupor and Coma