outcomes and are relatively insensitive to
metabolic derangements and drug effects.
36
Bilateral loss of primary cortical somatosensory
responses has been repeatedly confirmed to
have a 100% specificity for outcomes no better
than a permanent VS following anoxic in-
juries.
37,38
A recent review
23
found that of 176
patients with absent bilateral primary somato-
sensory responses (N20), none recovered past
a permanent VS (Table 9–9). The robust cor-
relation of bilateral loss of SSEPs and poor
outcome reflects a close connection with the
underlying degree of anoxic injury as indicated
by autopsy studies.
39
Of 10 patients examined
at autopsy who had SSEP measurements ob-
tained within 48 hours of cardiac arrest, all
seven with bilateral absence of the SSEPs had
extensive anoxic-ischemic destruction of the
cerebral cortex (with acute ischemic changes in
patients with short survival, and frank necrosis
of the pseudolaminar type in those patients
with longer survival times). Two additional
patients (one with delayed SSEPs and one with
normal-latency SSEPs) showed patchy neuro-
nal loss in the cerebral cortex. Importantly,
although an index of better outcomes, preser-
vation of normal-latency SSEPs following car-
diac arrest is not a definite predictor of positive
outcomes. Death or vegetative outcomes may
occur in as many as 40% of cases where a
normal N20 response is measured.
38
Other electrophysiologic techniques, includ-
ing EEG, brainstem auditory-evoked responses
(BAERs), and transcranial motor-evoked re-
sponses, also have predictive value (see
23
for
detailed review). EEG patterns are often sup-
pressed early following anoxic injuries and a
variety of signal abnormalities
22
correlate with
poor outcomes; these include burst suppres-
sion, alpha-theta patterns, and generalized sup-
pression or periodic patterns. The BAER test
can identify severe brainstem injury, but does
not address the outcome of cerebral cortical
injury. Preservation of longer latency auditory-
evoked responses that involve contributions
from larger cerebral cortical networks may pre-
dict recovery of cerebral function with greater
specificity. Both a late auditory response (N100)
and the mismatch negativity (MMN) response
have value in predicting outcome from coma
following anoxic injury.
40
Other longer latency
evoked responses such as the P300 and N400
have also been studied (see
22
for review).
PITFALLS IN THE EVALUATION
OF COMA FOLLOWING
CARDIOPULMONARY ARREST
Although prognosis in coma following cardio-
pulmonary arrest is generally accurate, pitfalls
do exist. The following case illustrates an ex-
treme, although not isolated, example from the
literature.
41
Patient 9–1
A 25-year-old asthmatic man collapsed at home
and stopped breathing. The patient received car-
diopulmonary resuscitation (CPR) from a family
member for 6 minutes until emergency medical
personnel arrived to find the patient without re-
spiratory effort or palpable pulse. Electrocardio-
gram (ECG) showed a rate of 24 bpm; CPR and
tracheal intubation were performed. Three min-
utes later the pulse was 107 bpm and spontaneous
respirations were noted. Initial GCS was 3. In the
Table 9–9 Somatosensory-Evoked Potentials in Anoxic-
Ischemic Encephalopathy: Absent N20 Response
Series
Day
Proportion
With Sign
Proportion
Recovering
Brunko and Zegers
De Byl, 1987
<
8 hours
30/50
0/30
Rothstein, 2000
<
2 hours
19/40
0/19
Madl et al., 2000
<
2 hours
22/66
0/22
Chen et al., 2000
1–3
12/34
0/12
Total
<
3
83/190
0/83
From Young et al.,
23
with permission.
354
Plum and Posner’s Diagnosis of Stupor and Coma
emergency room the patient was unresponsive
with dilated pupils that were responsive to light;
spontaneous decorticate posturing was noted. The
patient was sedated with propofol, given atracur-
ium, and transferred to the intensive care unit
(ICU). In the ICU the patient required mild pressor
support and was noted to exhibit frequent myo-
clonic jerks of the head and all four limbs. EEG
recordings revealed generalized status epilepticus.
Theophylline levels were within the normal ther-
apeutic range. Seizures were uncontrolled with
phenytoin, midazolam, clonazepam, valproate,
and MgSO
4
, so that thiopental infusion producing
burst suppression was required. After cessation of
the thiopental drip, generalized alpha frequency
activity was noted. On the sixth day the patient
was extubated, given a Do Not Resuscitate (DNR)
status, and transferred to the general neurology
floor still with a GCS of 3. He subsequently grad-
ually improved and had a GCS of 10 by day 16
with the recovery of head nodding and verbali-
zation. His GCS reached 15 by the 19th week
following the respiratory arrest. While EEG exam-
inations showed progressive improvements, the
patient continued to exhibit frequent myoclonic
jerks and epileptiform activity despite multiple an-
tiepileptic medication trials. Ultimately, this pa-
tient regained independent function.
This patient’s case highlights the potential
complexity of prognosis in coma even in circum-
stances that appear to predict poor outcome
following cardiac arrest and severe hypoxic in-
jury. A retrospective review of the history sug-
gests several points for consideration. While
the patient’s young age, initial presence of pu-
pillary light responses, and early return of spon-
taneous respiration were positive predictors,
the presence of myoclonus and seizures with
no history of epilepsy suggested severe hypoxic
injury. As reviewed above, postanoxic myoclo-
nus usually predicts a dismal prognosis,
42
but
this is not invariably the case.
43
The early se-
dation and paralysis of the patient due to the
seizure activity may have masked improve-
ment in level of consciousness within the first
6 hours, and the extensive use of different an-
tiepileptic medications may have mimicked the
pattern of alpha coma, a finding that otherwise
carries a greater than 90% mortality in the
setting of anoxic injury.
44
This patient demonstrates the limitations of
obtaining complete information from events
in the field and unequivocal separation of the
effects of primary injury versus potential con-
founds introduced by methods of treatment.
A pulseless patient may still have some unde-
tected circulatory activity, or have lost perfu-
sion just prior to evaluation, making accurate
estimate of duration of hypoxia problematic. A
similar case involving seizures and myoclonus
following a cardiac arrest has been reported,
with lateimprovement onday16 after remaining
at a GCS of 5 until that point.
45
Finally, a postictal state can severely depress
brainstem function, and tonic seizures can sim-
ulate flexion or extension posturing, whereas
single epileptic jerks can be difficult to distin-
guish from myoclonus. Cardiac arrest from a
seizure-induced cardiac arrhythmia
46
can fur-
ther complicate the picture.
Vascular Disease
STROKE
Prognosis in coma following stroke depends on
the arterial territory affected by the stroke that
produces bilateral hemispheric dysfunction as
detailed in Chapter 4. Wijdicks and Rabin-
stein
47
surveyed the literature of prognostic
factors for severe stroke from 1966 to 2003.
They found no evidence-based studies better
than class III to indicate prognosis, although
several suggestive clinical and radiologic fea-
tures were identified. Large proximal vessel
occlusions causing diffuse hemispheric edema
and midline shift carry a grave prognosis with a
nearly 90% mortality when the shift of the
septum pellucidum was greater than 12 mm.
48
Patients with coma caused by acute basilar oc-
clusions may recover
49
(see Chapter 2), whereas
those with coma due to hypertensive pontine
hemorrhages usually do not.
50
SUBARACHNOID HEMORRHAGE
Coma resulting from spontaneous subarach-
noid hemorrhage (SAH) has a grave prognosis.
The World Federation of Neurological Sur-
geons (WFNS) grades SAH using the GCS
51
(see also
52
) (Table 9–10). Although brief loss
of consciousness is common, coma is a rela-
tively uncommon sign in patients who reach
the hospital with SAH; two-thirds present
with WFNS grade III examinations or better.
Consciousness, Mechanisms Underlying Outcomes, and Ethical Considerations
355