downward pressure on the midbrain, resulting
in sudden lapse into deep coma.
Safety of Lumbar Puncture
in Comatose Patients
A common question encountered clinically is,
‘‘Under what circumstances is lumbar punc-
ture safe in a patient with an intracranial mass
lesion?’’ There is often a large pressure gradi-
ent between the supratentorial compartment
and the lumbar sac,
65
and lowering the lumbar
pressure by removing CSF may increase the
gradient. The actual frequency of cases in
which this hypothetical risk causes transtento-
rial herniation is difficult to ascertain. Most
available studies date to the pre-CT era, as cli-
nicians perform a lumbar puncture only rarely
after the presence of a supratentorial mass le-
sion of any size is identified. Several older
studies examining series of patients with brain
Eupneic
No
reaction to light
DOLL’S HEAD MANEUVER
ICE WATER CALORICS
Moderately dilated
Downward with full
lateral movements
Downward with no
upward movement
(bilateral cold water)
Appropriate motor
response to noxious
orbital roof
pressure
Bilateral
Babinski’s
Paratonic
resistance
Respiratory
pattern
a.
Pupillary
size and
reactions
b.
Oculocephalic
and
oculovestibular
responses
c.
Motor
responses
at rest
and to
stimulation
d.
Downward with full lateral movements.
Early
loss of upgaze and vergence
then downgaze.
Figure 3–15. Signs of dorsal midbrain compression.
112
Plum and Posner’s Diagnosis of Stupor and Coma
tumors who underwent lumbar puncture found
complication rates in the range of 1% to 2% in
patients with documented increased CSF pres-
sure or papilledema.
66,67
On the other hand,
of patients referred to a neurosurgical service
because of complications following lumbar
puncture, Duffy reported that 22 had focal
neurologic signs before the lumbar puncture,
but only one-half had increased CSF pressure
and one-third had papilledema.
56
The experi-
ence of the authors supports the view that
although lumbar puncture rarely precipitates
transtentorial (or foramen magnum) herniation,
even in patients who may be predisposed by
an existing supratentorial mass lesion, neither
the physical examination nor the evaluation of
CSF pressure at lumbar puncture is sufficient
to predict which patients will suffer compli-
cations. Hence, before any patient undergoes
lumbar puncture, it is wise to obtain a CT (or
MRI) scan of the cranial contents. If a patient
has no evidence of compartmental shift on the
study, it is quite safe to obtain a lumbar punc-
ture. On the other hand, if it is impossible to
obtain an imaging study in a timely fashion and
the neurologic examination shows no papille-
dema or focal signs, the risk of lumbar punc-
ture is quite low (probably less than 1%). Under
such circumstances, risk-benefit analysis may
well favor proceeding with lumbar puncture if
the study is needed to make potentially life-
saving decisions about clinical care.
False Localizing Signs in the
Diagnosis of Structural Coma
It is usually relatively easy for a skilled examiner
to differentiate supratentorial from infratento-
rial signs, and the cranial nerve findings due to
herniation syndromes are characteristic. How-
ever, there are a number of specific situations in
which the neurologic signs may falsely cause the
examiner to consider an infratentorial process
or to mistake an infratentorial process for one
that is supratentorial.
The most common false localizing sign is ab-
ducens palsy. This may be caused by increased
ICP, or it may occur after lumbar puncture. In
the latter case, the reduced CSF volume can
cause the brain to lose its usual buoyant sus-
pension in the CSF. The sagging of the brain in
an upright posture is thought to cause traction
on the abducens nerve. More rarely other cra-
nial nerves, including the trochlear, oculomo-
tor, or trigeminal nerves, may be similarly af-
fected.
Differentiation of supratentorial from infra-
tentorial causes of ataxia has presented a diag-
nostic dilemma since the earliest days of neu-
rology.
68
In the days before imaging, despite
highly developed clinical skills, it was not un-
usual for a neurosurgeon to explore the poste-
rior fossa, find nothing, and then turn the pa-
tient over and remove a frontal tumor. The gait
disorder that is associated with bilateral medial
frontal compression or hydrocephalus can be
replicated on occasion by cerebellar lesions.
Similarly, unilateral ataxia of finger-nose-finger
testing, which appears to be cerebellar in origin,
may occasionally be seen with parietal lobe le-
sions.
69
Another source of confusion is the differ-
entiation of upper (supranuclear) versus lower
motor neuron cranial nerve palsies. Although
rare, acute supratentorial lesions can on occa-
sion cause lower cranial nerve palsies (asym-
metric palate, tongue weakness on one side).
Bilateral supratentorial lesionscan produce dys-
arthria, dysphagia, and bilateral facial weakness
(pseudobulbar palsy, also called the opercu-
lar or Foix-Chavany-Marie syndrome
70
). Con-
versely, the well-known upper motor neuron
facial palsy (weakness of the lower part of the
face) can be seen with some posterior fossa le-
sions. The distinction between upper versus
lower motor neuron cranial nerve weakness
can often be made on the basis of reflex versus
voluntary movement. For example, a patient
with supranuclear bulbar weakness will often
show intact, or even hyperactive, corneal or gag
reflexes. A patient with an upper motor neuron
facial palsy will typically show a much more
symmetric smile on responding to a joke than
when asked to smile voluntarily.
Fortunately, these classic problems with
localization rarely intrude on interpretation of
the examination of a patient with an impaired
level of consciousness, as the signs associated
with herniation typically develop relatively rap-
idly as the patient loses consciousness. If the
patient displays false localizing signs while
awake, the progression of new signs that occur
during the herniation process generally clari-
fies the matter. Nearly all patients with im-
paired consciousness and focal brainstem signs
should be treated as structural coma and re-
ceive immediate imaging studies, so that any
Structural Causes of Stupor and Coma
113