Pain: Reflex Sympathetic Dystrophy Prevention and Management
Boca Raton, Florida
H. Hooshmand, M.D.
In our experience of over 100
patients suffering from electrical injuries referred to our clinic from
difference parts of the country, 42 patients had comprehensive extensive
studies, both anatomical and physiological.
The rest of the patients had the
majority of their studies done in other centers, and they are not included in
this series of 42 patients being reported because there was not a complete
battery of anatomical tests (MRI or CT), neuropsychometric tests (Halstead-Reitan
or Luria-Nebraska), and neurophysiologic tests (evoke potentials and topographic
The following is a summary of the
stereotypical clinical findings on electrical injuries. Thirty-three of 42
patients suffered from RSD. The treatment for the patients suffering from RSD
secondary to causalgic pain of electrical contact was quite difficult and taxing
to the clinician and to the patient.
As with other forms of RSD, the
disease is classified into four stages.
Stage I: On the Scene of the
phenomenon. This was present in practically every patient except for the
ones who had exposure to electricity to area that could not undergo gripping
of the hand, such as contact with the foot or dorsum of the forearm
(Figure5a). No-let-go phenomenon means the electrical stimulation causes
flexor spasm of the muscles, not allowing the victim to let go of the
2. Ipsilateral extremity burn, eschar, and neurosensory damage. The
same phenomenon to a lesser extent is present in the contralateral extremity
- exit point of the electricity. The lesion specifically involves c fiber
nerves and nerves around the arterioles (sympathetic nerve fibers) with
ephapse in c fibers. As a result, the patient has severe pain in the
involved areas, and the pain extends far beyond the eschar region.
3. The body is usually thrown away
from the source of electricity in one massive myoclonic jerk. This results
in falling from a ladder or other heights with secondary injuries.
4. Tonic and at times tonic clonic
seizures of brief duration, followed by a brief loss of consciousness.
5. Cardiac arrhythmias and
brief cardiac arrest with good response to resuscitation, followed by
typical autonomic dysfunction in the form of abnormal cardiac rhythm,
fluctuating blood pressure, and abdominal and chest pains. Attacks of apnea
are quite frequent.
6. Blisters over the fingers, acute
RSD of extremity, blisters and reddish discoloration over the contralateral
exit point, as well as blisters and reddish discoloration over the anterior
chest wall at T4 through T6 levels, which are the points of entrance of
electricity through vascular and sympathetic fiber to the spinal cord
Stage II: Hospitalization
1. The patient is
quite drowsy and at times confused and tried.
2. Labile vital signs in the first 24
hours, prolonged PQ, deep Q, irregular PQ interval, and arhythmias on EKG.
Orthostatic hypotension is quite common at this stage, resulting in syncopal
attack when the patient tries to get up and walk.
3. Akinetic attacks. Usually
myoclonic seizures are less frequent at the stage, and they are more likely
to develop in Stages III of IV.
4. Vertigo and tinnitus, which can
be quite intractable, lasting for months to years.
5. Painful extremities at the points
of entrance and exit, eschars of different degrees, and RSD.
6. Sensory loss over the trunk
distal to the T4 through T6 entrance of electricity to the spinal cord. This
sensory loss is usually asymmetrical, and the patient usually develops a
partial Brown-Sequard syndrome. This aspect of the examination should be
checked on every patient. This is the most frequently overlooked and
underdiagnosed sign of electrical injuries.
This sign of spinal cord injury
explains the reason for the patient having myoclonic and akinetic seizures
too deep to be recorded on EEG.
This is practically pathognomic and
was present in every patient.
7. Frontal lobe dysfunction: tremor,
positive snout reflex, masked fascies, irritability, and poor judgment were
present in over 50% of the patients.
Stage III: First Few Weeks
to Months after the Accident
pain, hyperpathia, and allodynia were present in 29 of 42 patients.
2. Akinetic or myoclonic seizures were
present in 28 of 42 patients.
3. Anxiety, agitation, phobia,
4. Labile neurovascular symptoms and
a. Cardiac arrhythmias
c. Labile blood pressure,
d. Abdominal cramps
f. Noncardiac origin chest wall pain
usually due to sympathetic nerve injury(Figures 4d and 4e).
5. Poor recall, poor recent memory.
6. Depression and secondary insomnia
were present in 28 of 42 patients.
7. Frontal lobe dysfunction,
irritability, tremor, poor judgment, poor tolerance, and fatigue.
Stage IV: Over 6 Months
1. Loss of job(
over 50% of the patients).
2. Loss of spouse, severe marital interpersonal strain(over
50% of patients).
3. Vertigo and tinnitus in one-third
4. Severe depression or
schizoeffective withdrawal, anxiety, phobia in over three-fourths of the
5. Akinetic and myoclonic seizures.
6. Poor recall and recent memory in
over 60% of the patients.
7. Painful extremity (chronic pain)
in over 30% of the patients.
8. RSD in 33 of 42 patients.
9. Impotence, neurogenic bladder,
abdominal cramps, and chronic tremor.
DIAGNOSTIC TESTS FOR ELECTRICAL
1. Anatomical tests,
i.e., MRI or CT scans are normal.
2. Physiological tests:
a. EEG usually is normal: 7 (14%)
patients had sharp transients, and 4 (9%) had epileptiform discharges in the
temporal frontal regions.
b. EKG abnormal in Stages I and II
in over 50% of the patients. The EKG subsequently reverted to normal.
c. Thermography was abnormal in 33
of 42 patients, showing different degrees of RSD (Figures 4d, 4e, and 25).
d. Evoked potentials.
i. Visual evoked potentials are
ii. Baer showed abnormalities in
interpeaks I-III in 30 of 42 patients and in 21 of 42 patients in stage IV.
iii. SSEP was normal in 39 of 42
patients in Stages I-III and 27 of 42 in Stage IV.
e. Topographic brain mapping was
abnormal in 28 of 42 patients in Stages III and IV.
None was done in Stages I and II.
The low percentage of EEG abnormality may be
due to (1) involvement of deep structures, and (2) tests done in late (chronic)
stages of the disease.
The abnormality on topographic brain mapping is
usually in the form of frontal temporal asymmetry and suppression of background,
which was bilateral in 22 of 28 brain mappings. In two patients,
a dislocation was noted. This phenomenon refers to
the fact that the a
frequency power spectrum has shifted from the occipital
lobes to the frontal lobes. These patients had suffered from prolonged coma
after the electrical injury. They suffered from a marked frontal lobe
dysfunction as mentioned above.
The only other condition that causes
on brain mapping is rare severe head injuries or cerebral anoxia, which shows "a
coma" on the EEG as well.
The electrical injury causes CNS damage and
follows the path of least resistance, which is the c fibers and the sympathetic
nerve fibers surrounding the arteries to the thoracic spinal cord. The damage
ascends up and sown to the lower portion of the spinal cord in the final
pathways of the nociceptive c fibers (Figures 4d-f, 25, and table 14).