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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_6042_Библиотеки_им_академика_М_И_Перельмана.pdf
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benzene in the nerve cells interferes with their normal metabolism, both in the brain as
in the spinal cord.
Normal metabolic activity and full functions only return after the complete elimination of
the aromatic hydrocarbons. However, this effect occurs slowly because of the high lipid
solubility of the hydrocarbons.
The neurotoxicity (Gerarde, 1959; Gerarde, 1960; Hine 1954) of the aromatic hydrocarbons
is believed to be a consequence of hemorrhage in the nerve system, principally in the
grey matter of the cervical and thoracic spinal cord.
These hemorrhages are believed to be the result of local irritation of endothelial cells of the
blood vessels, resulting in permeability changes in the capillaries. This in turn leads to
increased diapedesis, edema in the surrounding tissues, petechial and gross hemorrhages. Animal experiments showed paralysis of the extremities with fi nal destruction
of the nerve cells. Concerning the toxic effect on the nerve tissues Hine (1954) commented as follows, “on reviewing the literature we were surprised to fi nd no reference
to detail studies of central nervous system lesions by benzene.”
The authors diagnosed the case as transverse myelitis at C7-C8, T1 due to ben-
zene toxicity.
124.5 Clinical Picture
The patient was a 25 year old male who had chronic exposure to benzene and manifested by pain in the interscapular area, radiated to both arms and progressed to both
legs. In a couple of hours he had paresis of the upper limbs and complete paralysis
of the lower, i.e. quadriplegic, with hypotonic muscles. Parathesia and sensory distortion developed from T1 down. Bladder and bowel dysfunction was noted. Blood
picture and CSF studies were unremarkable. Myelography was negative for tumors
and somatosenory evoked potential (SSEP) indicated medullary injury.
124.6 Diagnosis
Diagnosis is based on the following criteria:
1. Patient’s history including occupational exposure to benzene
2. exclusion of other conditions: multiple sclerosis, tumors, Guillian-Barré syndrome,
viral infection, vascular malformation, syphilis, Pott’s disease, hematomyelia, polyarteritis nodosa, arachnoiditis, sarchoidosis, syringomyelia, spondilosis, etc.
3. Abnormally high urine phenol levels, with decreasing levels with improvement
of the patient.
124.7 Management
The case was managed conservatively, non-specifi cally, except the withdrawal from
the environment. He was exposed to the benzene fumes for many years. His condition improved and patient could walk without crutch, with some residual urinary
124 Benzene Myelitis
421
symptoms indicating Crédé’s technique and some weakness of the feet extensors 7
months after the onset. Phenol levels returned to normal.
Conclusion
This benzene neurotoxicity has been reported only once. More than two million
people are exposed to benzene and possibly a case may be encountered in the
industrial medical practice. Although very rarely, neurotoxicity affected the spinal cord giving the picture of transverse myelitis confi rmed by the urinary phenol
levels and by exclusion of other pathologies based on clinical data and laboratory
tests. When the inhalation is discontinued recovery is obtained although not quite
complete.
Reference
Herregods P, Chappel R, Mortier G. Benzene poisoning as a possible cause of transverse myelitis.
Paraplegia. 1984;22:305–10.
Reference
423
© Springer International Publishing Switzerland 2016
I.M. Eltorai, Rare Diseases and Syndromes of the Spinal Cord,
DOI 10.1007/978-3-319-45147-3_125
125
Myelopathy due to Flexion Drug Overdose
125.1 Definition
This is a condition of cervical myelopathy, developing after prolonged extreme neck
fl exion in association with profound muscular relaxation.
125.2 Incidence
Although cervical myelopathy may develop after prolonged neurosurgical operations, with the neck fl exed in the sitting position for occipital fossa lesions; this
condition is a different entity. The cervical myelopathy after prolonged extreme
fl exion of the neck has been reported twice by Kaye et al. ( 2001 ) and Nielsen and
Damek ( 2012 ).
125.3 Etiology
The fi rst case was caused by acute neck fl exion for 18 h with use of an overdose of
valporic acid. The second case was psychotic case with suicidal tendency and had
overdose of quetiapine fumarate, oxycodone/acetaminophen and chloral hydrate.
Prolonged neck fl exion may be fi xable action by criminals, e.g. robbery or prolonged assault.
Abstracted from Kaye et al. ( 2001 )
424
125.4 Pathophysiology
Prolonged neck fl exion may result in spinal cord damage, cervical myelopathy as in
the fi rst case and thoracic myelopathy as in the second case. The cause is not quite
clear, theories include:
• Vascular: the acute fl exion of the neck, stretching the arteries, and the veins of
the spinal cord, thus altering its autoregulation
• Neuronal or mechanical: the cord is injured by direct mechanical distraction by
compression or axial stretching
• Combination
– The ischemia may account for the central gray damage
– Mechanical stretching may cause the disruption of the axons in the white mat-
ter. In Nielsen and Damek case, there was also thoracic myelopathy.
The fi rst case expired and postmortem cord pathology showed dusky softening at
C5-C6 dislocation and softening of the entire cross sections. Microscopic exam
showed bilateral degeneration of the ascending tracts including gracilis, tractus
cuneatus, spinocerebellar, and spinalthalamic tracts. At C6, there was extensive
necrosis of the whole sectional area, with only small residual normal tissue around.
There was marked macrophages infi ltration; there was degeneration of C7 spinal
roots.
125.5 Clinical Picture
The type of patient, psychiatric, or an overdose of certain drugs. Prolonged sitting
with the cervical spine, markedly fl exed for many hours. Consciousness may be
veiled; tetraplegia with sensory-motor defi cits, and autonomic dysfunction, refl exes
exaggerated, Babinski’s sign is positive. There may be signs of pressure on the
ischial areas.
125.6 Diagnosis
Diagnosis based on:
1. History of kind of patient: the use of drugs, especially with overdose
2. Neurological exam
3. Laboratory tests: routine hematology, blood chemistry, and pharmacology
4. Spinal radiography
5. MRI abnormal cord signals of the cervical cord C4-C5 and possibly upper thoracic segments. Edema of the cord, with loss of fat planes on T2-weighted
images. Images show space occupying lesions.
6. Evoked potential sensory and motor show sensory and motor defi cits
125 Myelopathy due to Flexion Drug Overdose
425
125.7 Management
• Early diagnosis is important and keeping this pathology in mind
• The use of IV methylprednisolone to reduce edema, infl ammatory reactions,
excessive cytokine release, excitotoxic damage. However, it is still controversial;
it must be used within 8 h.
• Other promising products include monosialo-tetrahexo-synganglioside (AM-1)
and thyrotropin-releasing hormone
• Induced systemic hyperthermia in acute setting of spinal cord injury
Updating
Wang et al. 2012
Case report
A 56-year old male presented unable to move his limbs following drug overdose.
Neurological examination revealed C6 ASIA spinal cord injury. The CT of his cervical spine showed no fracture; however MRI showed cord edema extending from
C3-C6, as well as posterior paraspinal signal abnormalities, suggestive of ligamentous injury. He underwent a posterior cervical laminectomy and fusion from C3-C7.
The authors hypothesize likely due to existing cervical stenosis, in addition to overdose of sedating medication, which resulted in cervical spine vascular and/or neurological compromise producing an irreversible spinal cord injury.
Reference
Wang TS, Grunch BH, Moreno JR, Bagley CA, Gottfried ON. Drug overdose
resulting in quadriplegia. Eur Spine J. 2012;21 Suppl 4:S521–4.
References
Kaye KL, Ramsay D, Young GB. Cervical fl exion myelopathy after valproic acid overdose. Spine.
2001;26(19):E459–61.
Nielsen AS, Damek DM. Window of opportunity: fl exion myelopathy after drug overdose. J
Emerg Med. 2012;42(1):36–9.
References
427
© Springer International Publishing Switzerland 2016
I.M. Eltorai, Rare Diseases and Syndromes of the Spinal Cord,
DOI 10.1007/978-3-319-45147-3_126
126
Myelopathy due to Heroin Addiction
126.1 Definition
This is a myelopathy due to cocaine and/or heroin addition, whether by intravenous
use or intranasal insuffl ation or smoking or inhalation.
126.2 Incidence
Sporadic cases are reported periodically abstracted from McCreary et al. ( 2000 ). In
2000, McCreary reported a case of acute myelopathy following intranasal insuffl ation of heroin: a case report.
126.3 Etiology and Pathology
The use of illicit drugs is increasing. The toxic effects are well know to toxicology.
We will focus on spinal cord damage (myelopathy). Myelopathy can occur as a
result of the following:
• spinal cord ischemia due to infarctions resulting from hypotension
• direct toxic myelopathy
• toxic vasculitis with secondary myelopathy
Fux et al., 2003
428
• hypersensitivity causing edema and subsequent ischemia of the nerve cells, similar to what happens in the brain. This is seen in the fi rst use after abstinence. This
usually occurs via haptenation 1 of the drug with an in-vivo protein. In myelopathy, this may involve a specifi c protein to the spinal cord parenchyma causing
infl ammatory reaction, ischemia, and tissue injury.
• Infarction with septicemia
• combination of two or more factors
Myelopathy may be in the form of transverse myelitis or patchy areas of isch-
emia and cellular infi ltration.
126.4 Clinical Picture
This onset is usually acute and associated with other toxic effects of the drug, e.g.
toxic encephalitis, hepatitis, nephritis, myocarditis, myopathy, rhabdomyeloysis,
electrolyte imbalances, and coagulopathy. Myelopathy is diagnosed by neurological
signs, sensory and motor defi cit, and sphincter disturbances.
126.5 Diagnosis
1. History of drug use
2. Toxicology tests
3. hematological and biochemical testing
4. electrophysiological studies
5. CT scan shows cord edema and patchy hyperdensity
6. MRI of the spine: consists of acute transverse myelitis. T2-weighted images
show cord swelling with increased signals over most of the transverse diameter.
Enhancement is usually patchy. Gadolinium enhancement may occur acutely,
consistent with an acute infl ammatory process, disrupting the blood cord
barriers.
126.6 Management
• Detoxifi cation by antidote Narcan
• Cardiovascular stability
• respiratory care
• fl uid and electrolyte balance, transfusion if needed
• corticosteroids
• plasmapheresis or immunopheresis
1
Hapten is a small separable part of an antigen that reacts specifi cally with an antibody but is
incapable of stimulating antibody production except in combination with a carrier protein.
126 Myelopathy due to Heroin Addiction
429
• hemodialysis if needed
• in paraplegia, a rehabilitation program
Reference
McCreary M, Emerman C, Hanna J, Simon J. Acute myelopathy following intranasal insuffl ation
of heroin: a case report. Neurology. 2000;55(2):316–7.
Reference
431
© Springer International Publishing Switzerland 2016
I.M. Eltorai, Rare Diseases and Syndromes of the Spinal Cord,
DOI 10.1007/978-3-319-45147-3_127
127
Myelopathy due to Wasp Sting
127.1 Definition
The wasp is an insect of the hymenoptera order, which includes 100,000 species of
insects, including bees, ants, and wasps. These are known to be well developed in
social and colonial life. It is stated that four persons die every year in the UK due to
anaphylactic reaction to wasp or bee stings. Myelopathies recorded are mostly due
to Vaspa tropica stings.
127.2 Incidence
Myelopathy due to wasp sting is rare. Although, allergic reactions to wasp stings are
common; neurological complications are rare. However, myelopathy, encephalomyeloradiculopathy, cerebral infarction, optic neuropathy, polyradiculopathy,
encephaloraduloneuritis, and even myesthenia gravis have been reported. The
course of the illness may lead to partial or complete recovery, or may be permanent
and end fatally.
127.3 Etiology
The etiology of neurologic damage may be due to one or more of the following
factors:
• the venom contains no myelin proteins or peptides that cause allergic reactions
by producing certain antibodies that cross react with myelin basic proteins
Abstracted from Likittanasombut et al. ( 2003 )
432
• phosphalypaise-A activity of the venom may liberate encephalogenic basic proteins or other antigens from the myelin membraines of the central and peripheral
nervous systems inducing immune reactions
• vascular thrombosis, possibly due to vasoconsticition, secondary to release of
mediators released after wasp sting and possibly by platelet aggregation. The
venom also has infl ammatory and thrombogenic peptides and amines including
histamines, leukatrens and throboxane, the latter two are known to be
vasocontstrictors
However, there are possibly other mechanisms, which are not known.
127.4 Pathology
There is edema of the spinal cord with areas of demyelination in the cord and nerve
roots sometimes the picture of acute myelitis or acute encephalomyeloneuritis.
Patchy areas of gray and white matter demyelination, vascular changes, and cellular
infi ltration May develop due to vasoconstriction and by platelet aggregation.
127.5 Clinical Picture
History of a sting by a wasp, especially in endemic areas. The onset of symptoms is
within minutes or hours in up to 96 % of cases. Local reaction at the site of the sting
which varies in degree according to antigenecity and antibody reactions.
Occasionally, it develops into an anaphylactic shock. Myelopathy is manifested by
Numbness of the extremities, weakness, eventually paralysis (tetraplegia) with loss
of sensation and sphincter control. First it is hypo or arefl exic and later will be
hyperefl exic. The picture is modifi ed by the presence of encephalitis and radiculoneuritis, with encephalitis. There is decline of tonic-clonic seizures and cerebral
paresis, respiratory distress, hypoxia, and possibly respiratory failure.
127.6 Diagnosis
1. There is hyperglobulinemia, throbocytopenia and high ESR.
2. CSF shows monocytosis
3. IgE antibodies to wasp venom are positive
4. Renal and hepatic function may be low
5. EKG may show cardiac ischemia
6. MRI shows ill-defi ned scattered lesions in the cervical cord, hypotensive signals
in T1-weighted images involving both the gray and white matter of the cervical
cord and in case of encephalopathy, the brain and brain stem may be involved.
7. Sensory conduction studies may be altered in radiculopathy and peripheral
neuropathy.
127 Myelopathy due to Wasp Sting