Download Neurologic Complications of Sit-Ups Associated With the Valsalva

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CLINICAL NOTE
Neurologic Complications of Sit-Ups Associated With the
Valsalva Maneuver: 2 Case Reports
Lori D. Uber-Zak, DO, Y. Swamy Venkatesh, MD
ABSTRACT. Uber-Zak LD, Venkatesh YS. Neurologic
complications of sit-ups associated with the Valsalva
maneuver: 2 case reports. Arch Phys Med Rehabil 2002;83:
278-82.
We present 2 cases of potentially catastrophic neurologic
consequences occurring in healthy individuals engaged in
sit-up exercises. Two young healthy men were engaged in
sit-ups when one developed a stroke and the other developed a
spinal epidural hematoma. The Valsalva maneuver involved in
the sit-up exercise can produce supraphysiologic increases in
blood pressure, which can lead to vascular injury and serious
neurologic consequences. Proper breathing should be encouraged and patients with known predisposing factors should
avoid such exercises. Prompt recognition of neurologic signs
and symptoms during exercise can be life saving. This is the
first report of the neurologic complications of sit-ups.
Key Words: Abdominal muscles; Case report; Cerebrovascular accident; Exercise; Hematoma, epidural; Rehabilitation;
Valsalva’s maneuver.
© 2002 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and
Rehabilitation
IT-UP EXERCISES ARE COMMON abdominal exercises
performed every day without adverse consequences by
S
many people for both fitness and rehabilitative purposes. However, performing the Valsalva maneuver during the exercise is
associated with a supraphysiologic increase in blood pressure.
In addition, the usual hypotensive phase may also be absent.
These 2 elements, combined with the significant rise in intraabdominal pressure, may be detrimental. We present 2 cases
with potentially catastrophic neurologic consequences that occurred in young, previously healthy patients engaged in this
activity. The cases, presumed pathophysiology, and a review of
the pertinent literature are discussed.
CASE DESCRIPTIONS
Case 1
A 37-year-old, right-hand dominant, healthy, white male
professional had been doing very rapid and strenuous sit-ups
when he developed the sudden onset of right-sided uncoordination, weakness, and sensory loss. By his description of the
exercise, he had been doing the Valsalva maneuver with the
sit-ups.
From Dept of Neurology, Loma Linda University, Loma Linda, CA (Uber-Zak);
and the Div of Neurology, Penn State College of Medicine, Hershey, PA (Venkatesh).
Accepted in revised form February 26, 2001.
No commercial party having a direct financial interest in the results of the research
supporting this article has or will confer a benefit upon the author(s) or upon any
organization with which the author(s) is/are associated.
Reprint requests to Lori Uber-Zak, DO, Dept of Neurology, Loma Linda University, 11370 Anderson St, 2400, Loma Linda, CA 92354.
0003-9993/02/8302-6514$35.00/0
doi:10.1053/apmr.2002.27378
Arch Phys Med Rehabil Vol 83, February 2002
The patient’s medical history and family history were unremarkable. He took no medications, denied tobacco abuse or
drug use, and admitted only to occasional social alcohol use.
On the previous night, he had ingested several beers, which
was unusual for him.
On examination in the emergency room, the patient was
afebrile, his blood pressure was 121/70, and his heart rate was
regular at 83. He was awake, alert and oriented times 4, and in
mild distress. Examination revealed no carotid bruits, and the
heart had a regular rate and rhythm without murmur.
The neurologic examination was remarkable for a mild right
upper motoneuron facial droop, a right homonymous hemianopia, and decreased sensation on the right side of the face.
There was a mild hemiparesis with motor strength, as graded
by the Medical Research Council (MRC) Scale, in the right
upper-extremity upper motoneuron muscle groups in the 4 to
4⫹/5 range and in the right lower-extremity upper motoneuron
muscle groups in the 4⫹ to 5⫺/5 range. Decreased proprioception and light touch were noted in the right hemibody. The
deep tendon reflexes (DTRs) were 1⫹/4 in the right upper
extremity but 2⫹/4 elsewhere with plantarflexor responses;
there was a right pronator drift.
Admission laboratory data revealed a white blood cell
(WBC) count of 13.7, a normal hemoglobin, hematocrit, platelet count, electrolyte panel, prothrombin time (PT), and partial
thromboplastin time (PTT). Computed tomography scan of the
head without contrast showed the left lateral ventricle to be
slightly effaced with no evidence of acute hemorrhage or
obvious infarct.
He was admitted and was started on aspirin 325mg/d. By the
following morning, there was slight improvement of his hemiparesis and his WBC count had normalized. Echocardiogram,
carotid duplex ultrasonography, and electrocardiogram (ECG)
were all normal. A magnetic resonance imaging (MRI) scan of
the head revealed an acute infarct of the medical inferior left
occipital lobe and posterior left thalamic region. An extensive
hypercoagulable work-up was performed, which was ultimately negative. On the fourth hospital day, the patient developed a headache and worsening of his original symptoms. A
head computed tomography scan was negative for blood, and
the patient was started on intravenous heparin. By the next
morning, the headache resolved. A 4-vessel cerebral angiogram
and review of the films with the neuroradiologist revealed
evidence of a complete occlusion in the lumen of the left
posterior cerebral artery.
Warfarin (Coumadin) was added for long-term anticoagulation with a goal of 1.5⫻ the baseline PT.
The patient remained stable throughout the remainder of his
hospital stay. He was discharged on Coumadin 5mg/d. He was
fully ambulatory and his motor strength had normalized. He
still exhibited a right homonymous hemianopia and a mild
subjective decrease in sensation in the right hemibody. He was
referred for outpatient rehabilitation.
Case 2
A 30-year-old healthy, black man was performing “hard, fast
sit-ups for a really long time” on the morning of admission. By
NEUROLOGIC COMPLICATIONS OF SIT-UPS, Uber-Zak
his description, he was not breathing with every cycle given the
speed of the exercise. During the course of this exercise, he
developed severe neck pain, which radiated to his upper chest,
shoulders, back, and head. He also noticed weakness of the
upper and lower extremities that rapidly progressed to bilateral
lower-extremity paralysis and a tingling sensation from his
chest to his feet.
The patient had no medical, surgical, or contributory family
history. He denied any tobacco or drug use, but admitted to
consuming approximately 4 to 6 beers a day. However, he had
not consumed any beers on the day of the incident. He was
taking no medications and his review of systems was otherwise
unremarkable.
On arrival the patient was afebrile, with a pulse of 49,
respiratory rate of 18, and blood pressure of 208/117. The neck
was tender along the cervical paraspinal muscles. Neurologic
examination revealed normal mental status and cranial nerve
examinations. His motor examination, using the MRC Scale,
revealed 5/5 shoulder abduction bilaterally, 4/5 elbow flexion
bilaterally, 3/5 wrist extension bilaterally, and 3⫺/5 elbow
extension on the right, with 3/5 on the left. All other upper- and
lower-extremity muscle groups were 0/5. On sensory examination, there was a mild decrease to pinprick at C8 –T1 on the
right with no pinprick sensation below T4. Proprioception was
absent in the left foot but present on the right. His DTRs were
2⫹/4 in the biceps brachialis bilaterally, with all other DTRs
being absent. Plantar responses were flexor bilaterally and
rectal tone was decreased. The general physical examination
was otherwise unremarkable.
Laboratory data revealed a normal complete blood count,
PT, PTT, and chemistry panel; ECG was sinus rhythm at 68,
and a urine drug screen and chest radiograph were negative.
Cervical spine MRI showed an extradural, elliptic mass of
high-signal intensity on T2-weighted images extending from
C5 to T1, with compression of the cord and extension into the
neural foramina at those levels.
The patient was started on dexamethasone. He underwent an
emergent decompression and evacuation of a spinal epidural
hematoma without complications. By postoperative day 12, he
was continent of bowel and bladder and independent in his
sitting balance. He was able to ambulate with a single-point
cane with only mild difficulty with balance owing to a slight
decrease in proprioception in the bilateral lower extremities.
He was discharged to home with outpatient therapy.
DISCUSSION
Sit-up exercises involve contracting the abdominal muscles,
lifting the trunk off of the floor, and bringing the trunk into the
flexed position. This exercise may involve the Valsalva maneuver during the concentric contractile phase, which is especially accentuated by improper breathing during this phase.
Even though athletes are commonly taught to exhale with
contraction or “blow up the weight,” many do not consistently
practice good technique. Also, sit-ups are such a familiar
exercise that many untrained people wanting to become fit will
often perform this exercise without proper knowledge of
breathing cycles.
The Valsalva maneuver creates an increase in intrathoracic
pressure and an increase in arterial blood pressure (ABP).1 It
has been found that the larger the amount of muscle mass
involved with an exercise, the larger the peripheral vascular
resistance and the higher the blood pressure that is generated.2,3
It has also been shown that although increases in blood pressure occur with resistance exercise, these increases were larger
when the exercise was performed with the Valsalva maneuver.2,3 The increase in blood pressure was closely associated
279
with the actual muscle contraction and/or the duration of the
Valsalva maneuver.2 Also, it is likely that the force produced
by the muscle contraction per se is part of the mechanism of the
increased blood pressure.2
The Valsalva maneuver has 4 distinct phases.1 In phase 1,
which is the beginning of the strain, there is a transient increase
in the ABP secondary to the transmission of the increase in
intrathoracic pressure. The early part of phase 2 is marked by
a fall of the ABP caused by impaired atrial filling of the heart.
This precipitates a sympathetically mediated increase in the
heart rate and ABP via the carotid sinus baroreceptors in late
phase 2. Phase 3 occurs when the strain is released. This is
marked by a sudden decrease in intrathoracic pressure, which is
transmitted to the arterial tree with a subsequent transient
decrease in the ABP. This is immediately followed by phase 4,
which begins with an overshoot of the ABP above the baseline
because sympathetic tone and systemic vascular resistance
remain elevated after atrial filling has normalized. This increase in blood pressure once again acts on the baroreceptors,
resulting in a transient bradycardia before baseline conditions
are restored.1
In addition to the physiologic changes described earlier, the
Valsalva maneuver also impedes venous return.4 Therefore, the
peripheral venous pressure can be higher than the right atrial
pressure.5
As well as ABP and venous return, the Valsalva maneuver
can affect the cerebral circulation.1 For example, the Valsalva
maneuver has been known to cause fainting and aneurysmal
rupture with subarachnoid hemorrhage, by virtue of its effects
on the cerebral circulation.1 Tiecks et al1 examined the effects
of the Valsalva maneuver on the cerebral circulation. In recording several parameters during the Valsalva maneuver, they
showed a relatively sharp increase in the cerebral blood flow
velocity (CBFV). CBFV can consistently overshoot the baseline reference point (by a mean increase of ⬎50% above
baseline with a maximal value in their study of approximately
100%). The combination of the simultaneous increase in ABP
and the decrease in the “protective” effects of the extravascular
cerebrospinal fluid pressure resulted in a major increase in the
transmural pressure gradient. Tiecks1 hypothesized that this
stage (ie, stage 4) of the Valsalva maneuver was that which
held the highest risk for such entities as tissue damage and
aneurysmal rupture in susceptible subjects. Two studies1,6 have
shown that cerebral autoregulatory mechanisms do not act
instantaneously and thus are not rapid enough to maintain a
constant cerebral perfusion pressure during the Valsalva maneuver.
It has been shown that the position of the trunk during the
Valsalva maneuver can influence the degree of increase in
intra-abdominal pressure.7 Significantly higher pressures were
shown to be generated when the Valsalva maneuver is performed with the trunk in a forward flexed position (ie, as
opposed to standing or flexion with rotation).7 The forward
flexed position is also the position that the trunk assumes in the
concentric phase of the sit-up exercise. Performing the Valsalva maneuver during repetitive resistance exercises, a grouping to which repetitive sit-ups can be ascribed, alters the
physiology of the Valsalva phases previously described. Phases
2 and 3, the hypotensive phases, do not occur with repetitive
resistive exercise; thus, blood pressure becomes augmented
throughout the repetitions. Not surprisingly, the highest blood
pressures have been observed in the final repetitions.2 ABP
elevations have been shown to reach into a supraphysiologic
range (ie, triple) during heavy resistance exercises, especially
when combined with the Valsalva maneuver (eg, readings of
Arch Phys Med Rehabil Vol 83, February 2002
280
NEUROLOGIC COMPLICATIONS OF SIT-UPS, Uber-Zak
up to 370/360mmHg recorded during maximal bilateral leg
press with the Valsalva maneuver).2
DISCUSSION
Both cases presented earlier involved young, otherwise
healthy men in their 30s, engaged in sit-up exercises at the time
of their respective events. We believe that the neurologic
events that occurred during the exercise were a consequence of
the sit-ups and not just a mere coincidental occurrence.
Thus, the pressure increases during the Valsalva maneuver
may have been enough to produce damage to the blood vessel
walls of these patients. Presumably, their respective events
occurred at the given anatomic sites because of a preexisting
weakness of the blood vessel wall.
In case 1, we believe that this patient’s stroke was caused by
focal damage to the blood vessel wall secondary to the high
intravascular pressures generated during the sit-ups. More specifically, we believe that this was an intracranial dissection of
the posterior cerebral artery. We hypothesize that a transient
rise in cerebral perfusion pressure during severe physical
stress, such as this, accompanied by a minor defect in the
elastic lamina, could initiate dissection.8
Intracranial dissecting aneurysms tend to occur in young
patients (late 20s to early 40s).8-11 The patients are rarely
hypertensive or have a history of atherosclerotic peripheral
vascular disease or diabetes.10 Ischemic infarction is the most
frequent clinical outcome that results from dissection.12 Although not specific for dissection, headache is a hallmark
symptom of dissection.10,13 Before anticoagulation, our first
patient experienced a progression of his symptoms, with concomitant headache, which was halted with heparin.
Also in favor of a dissection is the fact that the stroke
occurred during vigorous exercise involving the Valsalva maneuver. Exercise and stroke are known to have a small but
definite association.14 Exercise-induced arterial hypertension
related to the Valsalva maneuver is the presumed mechanism
of hemorrhagic stroke in weight lifters.2 Dissection of the
craniocervical arteries is a well-documented mechanism by
which exercise-induced stroke can occur.14 Cerebral infarction
in young or middle-aged patients with a history of recent
vigorous exercise increased the likelihood of the diagnosis of
dissection in 1 study even before angiography.14 Various sports
and activities have been noted to precede arterial dissection.14
Among these are swimming, archery, yoga, calisthenics, skiing, basketball, sliding into a base (baseball, softball), wrestling, volleyball, running, paddleball, surfing, trampoline jumping, and weight lifting.2,14-17 More specifically, intracranial
dissection has also been preceded by unusual exertion18 or
vigorous exercise (eg, vigorous walking, tug-of-war,8 vigorous
bicycle riding,19 weight lifting,10 ice hockey, strenuous basketball20). The association between strenuous physical exertion
and dissection may be an expression of an elevated arterial
pressure.9
Intracranial arteries lack an external elastic membrane and
have a thinner adventitia, fewer elastic fibers in the media, and
generally a thicker internal elastic lamina than the extracranial
arteries.10 The internal elastic lamina is the most important
layer in determining the strength of the intracranial arterial
walls.10 The vessels may be more prone to damage if the elastic
tissue is defective or deficient.10 Absent a primary vasculopathy, it has been suggested that dissection might arise as a result
of vessel wall weakening from gap defects in the internal
elastic lamina.8,10,12,18 It is not known whether such defects are
congenital or acquired.10
Additionally, this patient had no other cause for a thrombotic
stroke after a thorough work-up had been performed. Although
Arch Phys Med Rehabil Vol 83, February 2002
the angiogram showed an occlusion, it was performed more
than a week after the initial event. Angiographic findings of
intracranial dissecting aneurysms of the posterior circulation
are diverse, ranging from complete occlusion (eg, as seen in
our patient) to irregular narrowing of variable extent with or
without accompanying dilatation.10 This delay may have prevented us from assessing the original morphology of the arterial lesion because it may have changed from an initial and
more pathognomonic form by the time the test was performed
(ie, double lumen sign) to occlusion.21 Occlusion is among the
most common angiographic findings in dissection.9 The double
lumen sign is actually rarely seen in intracranial dissections of
the posterior circulation.10 Again, this is consistent with our
case.
Definitive diagnosis of intracranial dissecting aneurysms is
often difficult in the absence of pathologic confirmation.22 As
such, dissecting aneurysms of intracranial arteries may occur
with greater frequency than the literature suggests.22 Dissection
should be given careful consideration in young adults with
focal neurologic complaints or unrelenting headache or neck
ache after exercise14 and with no predisposing risk factors for
an atherosclerotic or embolic source.13
Our second patient developed a spinal epidural hematoma
(SEH) while doing sit-ups. SEH is a rare clinical entity reported only sporadically in the literature23-30 and is a neurologic
and neurosurgical emergency.23 The clinical presentation is
quite consistently a picture of the acute onset of localized back,
neck, or interscapular pain. This is usually followed rapidly by
a pattern of radicular pain in the extremities and chest, as well
as signs and symptoms of spinal cord or cauda equina compression.28,30-35 The initial pain is usually localized and is
referable to the level of the lesion,28,30-35 but quickly spreads.
The spinal epidural space contains an extensive internal
venous plexus, which communicates with the external vertebral
venous plexus; together they form Batson’s plexus. This is a
valveless low-pressure system.29,34 The spinal epidural venous
system provides an alternate route for venous return from other
areas of the body and assists in regulating volume and pressure
changes between the intrathoracic, intra-abdominal, intracranial, and intraspinal systems.23 Cerebral blood flow can use this
system for venous return when intrathoracic pressure is increased and the return flow via the jugular venous system is
impeded.23
Spinal epidural hematomas occur as a result of a number of
etiologic possibilities.32,35 Besides trauma,23,27,29,30,35,36 “trivial
trauma,” and spontaneous and idiopathic events,23,25,29-32,35
many seemingly trivial, common, daily events (eg, sneezing,
coughing, bending, twisting, vomiting, straining to void or
stool) have been the antecedent event to SEH and have been
implicated as causative.29,30,32,34,35 Many of these events, including sit-ups, involve the Valsalva maneuver34 (eg, straining,
coughing, lifting), and, thus, increase intra-abdominal and intrathoracic pressure.32,34,35 This, in turn, is transferred to the
spinal epidural venous system28,35 and is thought to contribute
to the rupture and hemorrhage of the epidural venous vessels.27,29 Interestingly, the pain accompanying a spinal epidural
hematoma increases dramatically with maneuvers that elevate
the pressure in the vertebral venous plexus (eg, coughing,
sneezing, straining).23
Thus, the common occurrence of such antecedent normal
events suggests that there must be some underlying pathologic
process or factor contributing to the etiology of the SEH32,35
(eg, underlying venous malformations and angiomas24). However, some have considered vascular malformations to have an
insignificant role in the etiology of SEH.30 The basic pathophysiologic origin is presumed to be a weakened vessel in a
NEUROLOGIC COMPLICATIONS OF SIT-UPS, Uber-Zak
preexisting abnormal venous plexus.33 The valveless nature of
the epidural venous plexus has been thought to leave it vulnerable to abrupt changes in pressure and thus subject to rupture.27,29,34
Prognosis in spinal epidural hematomas depends on prompt
recognition and management.30 The clinical history should
suggest the diagnosis.29 The knowledge that the patient had
recently performed sit-ups or some other exercise may help to
elucidate the etiology. Presumably, our second patient had a
preexisting abnormality in a blood vessel wall which, when
combined with the previously described blood pressure elevations with the Valsalva maneuver, left him vulnerable. We
believe that the Valsalva maneuver during the sit-up exercises
was the provocative factor. This is not unlike the mechanism of
cerebral hemorrhages that have been documented in weight
lifters2 or cases of vitreous and choroidal hemorrhages that
have been reported in association with the Valsalva maneuver.37-39 Spontaneous SEH should be considered in the differential diagnosis of severe neck pain in patients engaged in
physical activity (eg, swimming)34 and in the differential of
nontraumatic neck pain and spinal cord compression.27
A final possible confounding factor in these cases is alcohol.
Central nervous system events, including stroke, have been
noted to occur more commonly after alcohol ingestion. Alcohol
has been associated with both an increased and decreased risk
of stroke.40 The literature reveals the existence of a U- or
J-shaped curve for strokes and alcohol with chronic low consumption associated with a decreased risk and chronic heavy
consumption being associated with an increased risk.41 There is
also evidence that heavy binge drinking can increase the risk
for subarachnoid hemorrhage42 or of cardioembolic stroke in
patients with a known source.43 Our first patient had an ischemic stroke, and there was no known source of embolus after
an extensive work-up. Also, no literature exists on the rare
social drinker who has a few drinks—less than what would
qualify as a binge—and then has a stroke. Additionally, in a
recent meta-analysis,44 a high risk was noted between alcohol
and hemorrhagic stroke but the risk for ischemic stroke was
found to be independent of alcohol intake. Also, no literature
exists for a relationship between alcohol and spinal epidural
hematoma. Therefore, even though both of these patients had
consumed some alcohol on the day before the event, it is
doubtful that this alone would have lead spontaneously to
either event without a superimposed Valsalva from the sit-ups.
CONCLUSION
Sit-up exercises are commonly performed by many people
each day. We acknowledge that events such as those documented here are rare. However, neurologists and other physicians should be cognizant that the differential diagnosis of
neurologic signs and symptoms in healthy, young people engaged in exercise includes these serious entities. Early recognition of these conditions can influence neurologic outcome.
These cases bring to attention the physiology of the exercise
and the abnormal forces created. As noted earlier, the risks of
the Valsalva maneuver are well known in the athletic world.
These cases also force us to acknowledge that many people do
not breathe properly during exercise, which can lead to serious
consequences. We believe that these 2 cases should serve as a
reminder to physicians, nurses, physical therapists, and trainers
of the importance of proper breathing during resistance exercise. People with baseline hypertension or known vascular
anomalies should be particularly careful when performing any
act involving the Valsalva maneuver, including sit-ups. This
concept also possesses implications for the rehabilitation set-
281
ting where these types of forces may be even less well tolerated.
Acknowledgments: The authors thank Mark Kritchevsky, MD,
for his helpful comments.
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