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Cerebrospinal fluid monoamine metabolites in narcolepsy Reanalysis.

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LETTERS
Dangers of Lumbar Spinal
Needle Placement
Dewey A. Nelson, MD, FACP
Spinal punctures are usually performed at the L4-L5 or L5-
s1 interspace. The current trend toward performing “high”
spinal punctures probably entered neurology through teachings received by neurology residents on rotations through
neuroradiology. The L2-L3 interspace is often used during
myelography and is advocated in recent neuroradiology textbooks El, 21. In the text edited by Ramsey 121, the L2-L3
interspace is recommended, with the caveat that “fluoroscopic control” should always be used.
This departure from usual standards of spinal punctures
raises concerns, particularly in light of two recent case histories and radiographs which I reviewed from outside this
geographical area. Both of these young adults developed
conus medullaris syndromes during myelography. Needle
placement in both instances was at L2-L3. In addition, the
cephalic angulation of the spinal needles placed the needle
tips another half interspace higher or more. During followup, magnetic resonance imaging (MRI) in one patient revealed an enlarged conus medullaris, and a lesion was
identified and described as either a benign tumor or a cavitary lesion. On MRI it is difficult to identify the tapered
termination of the conus medullaris which is concealed by
spinal fluid that emits a high signal. During an attempt to
visualize the tip of the spinal cord by computed tomography
(CT), the conus appears higher than it really is owing to
volume averaging.
Work by Reimann and Anson 131 in 1944 and a careful
review by Dripps and Vandam (41 in 1951 remain cogent. It
was found, in dissections of more than 800 specimens, that
the usually accepted termination of the spinal cord (at L-1 to
upper half of L-2) is the apogee of a bell-shaped curve of
normal biological variants. The spinal cord terminates below
mid-L2 in 3 1% of normal individuals and may lie as low as L3 in 2%% 131. Similarly,Taveras and Morello [5] stated that
the termination of the conus medullaris may normally lie 4
cm higher or lower than at LI-L2.
Many physicians are now using the “European” or “Bellevue” spinal tap in which the patient is seated with elbows
upon thighs, with the spine acutely flexed. This draws the tip
of the conus cephalad and broadens the canal. This maneuver
creates high hydrostatic pressure (300-700 mm HzO) such
that the various ligaments and meninges are easily identified.
When resistance is lost, one can assume that the epidural
space has been entered. The “blade” of the bevel should be
turned parallel to the long axis of the spine to avoid cutting
the meninges. Then, by using the technique of “push and
test,” the needle is advanced no more than 2 mm at a time,
after which the stylet is withdrawn: the physician must wait
10 seconds between “tests” because the bevel of the needle
presents a minuscule pathway to the spinal fluid when the
arachnoid membrane is first perforated. With experience, it
is possible to place the needle’s bevel just inside the arachnoid. One must avoid crossing the entire canal for reasons of
patient safety. Often overlooked is the routine of replacing
the stylet, then giving the needle a half turn before finally
removing it. This ensures that no strand of arachnoid will be
threaded back through the dura to produce prolonged spinal
fluid leakage. The spinal needle is rarely displaced when the
patient is carefully tilted into the lateral decubitus position.
Interestmgly,when the L4-L5 interspaceis used, it gives one the
impression that the tent-shaped interspinous ligaments guide
the needle; by contrast, the space at L5-S1 seems to be loose
or unstable, allowing sideways drift of the spinal needle.
Section of Neurology
The Medical Center of Delaware
Wilmington, DE
References
1. Shapiro R. Myelography. Chicago: Year Book, 1984:60
2. Ramsey RG. Neuroradiology. Philadelphia: WB Saunders, 1987:
676
3. Reimann AF, Anson BJ. Vertebral level of termination of the
spinal cord with report of a case of sacral cord. Anat Rec 1944;
88:127-138
4. Dripps RD, Vandam LD. Hazards of lumbar puncture. JAMA
1951;147:1118-1121
5. Taveras JM, Morello F. Normal neuroradiology. Chicago: Year
Book, 1979:503
Cerebrospinal Fluid
Monoamine Metabolites
in Narcolepsy: Reanalysis
Kym F. Faull, PhD,* Christian Guilleminault, MD,”
Philip A. Berger, MD, and Jack D. Barchas, MDX
Reanalysis of an earlier publication (1) showed that the control group included 14 subjects who were recruited for a
different protocol than the rest of the control subjects. A
revised analysis of the “before probenecid” data, after elimi-
Concentration of Free Monoamine Metabolites (nglml)
in Human Lumbar Cerebrospinal Fluid
Before Probenecid Administration
Subject Groups
Metabolite
N”
Meanb
SE
Normal controlsb
DOPAC
HVA
MHPG
5-HIAA
DOPAC
HVA
MHPG
5-HIAA
23
26
26
26
0.45
37.9
8.7
22.7
0.40
37.4
9.7
30.1
0.08
3.4
0.7
2.2
0.03
2.3
0.7
2.3
Narcoleptics
5
6
6
6
“One-way analyses of variance of the before probenecid values for
each metabolite showed no significant differences ( p < 0.05) between subject groups or between the normal subjects and the combined groups of patients.
”Twenty-six male subjects (age: 20-59 years, mean 32.3; height:
143.5-190.5 cm, mean 169.3 cm; weight: 60.3-102.1 kg, mean
73.2 kg).
DOPAC = 3,4-dihydroxyphenylaceticacid; HVA = homovanillic
glycol; 5-HIAA
acid; MHPG = 3-methoxy-4-hydroxyphenylethylene
= 5-hydroxyindoleacetic acid.
310 Copyright 0 1989 by the American Neurological Association
nation of the 14 cases and some minor corrections to the
narcoleptic group, is given in the Table. These changes make
no material difference to the results or conclusions given in
the original manuscript, but in the interest of accuracy we
feel it is important to describe them.
*Department of Psychiatry and Behavioral Sciences
Stanfard Univwsity School of Medicine
Stanford, CA
Reference
1. F a d KF, Guillerninault C , Berger PA, Barchas JD. Cerebrospi-
nal fluid rnonoamine metabolites in narcolepsy and hypersornnia.
Ann Neurology 1983;13:258-263
patient seropositive for HTLV-I. The nature of the association between HTLV-I and TSP has yet to be explained and
its putative role in polymyositis requires further confirmation
and study. The long delay from the onset of the myelopathic
symptoms to the appearance of the polymyositis in our patient suggests differing pathogenic mechanisms. Direct neurotropic infection might be more important in TSP, whereas
the escape of autoimmunity from normal suppressor mechanisms is a more likely mechanism for polymyositis.
Department of Neurology
Guy’s Hospital
London, UK
References
Polymyositis and HTLV-I
Antibodies
D. A. Francis, MD, and R.A. C. Hughes, MD
Human T-lymphotrophic virus type I (HTLV-I) is established as an important etiological agent in 80% of patients with tropical spastic paraparesis (TSP) 111. A recent
study has shown an additional possible correlation between
HTLV-I seropositivity and polymyositis in Jamaican patients
[2]. The Trinidadian woman with HTLV-I antibodies described in the study has both conditions.
At age 32 she developed mild weakness in her lower limbs
associated with a tendency to trip and frequent falls. She
came to the United Kingdom at age 39 and presented at age
44 with a 9-month history of progressive limb girdle weakness and muscle tenderness but no sensory symptoms. There
was no relevant family history. Examination revealed weak,
tender proximal limb muscles. Her deep tendon reflexes
were brisk, abdominal reflexes absent, and plantar responses
extensor. There were no cranial nerve or sensory abnormalities. Investigations showed normal blood count, and erythrocyte sedimentation rate, and thyroid function, and the autoantibody screen was negative. HTLV-I antibodies were
positive (the particle agglutination test: positive; ELISA
method; titer, 1:256,000) and creatine kinase (CK) was increased to 1,276 U/L (normal < 205). The cerebrospinal
fluid contained 2 lymphocytes per microliter, protein was 15
mg/dl, and IgG was 7.2 mddl with IgG/albumin ratio 0.43
(normal < 0.2 1). Electromyography revealed frequent lowamplitude polyphasic potentials, and a deltoid muscle biopsy
showed focal necrosis and mononuclear cell infiltrates, consistent with polymyositis. Myelography was normal. A magnetic resonance image brain scan (T2 weighted) demonstrated multiple small focal areas of altered signal throughout
the white matter of both cerebral hemispheres consistent
with demyelination. On high-dose alternate-day prednisolone her muscle symptoms almost completely remitted and
the CK returned to normal. Now aged 49, she remains well
but stergid dependent; symptoms recur when the prednisolone dose is reduced below 10 mg on alternate days.
This patient fulfills the diagnostic requirements for both
tropical spastic paraparesis and polymyositis. To our knowledge this combination has not been reported before in a
1. Roman GC. The neuroepidemiology of tropical spastic parapa-
resis. Ann Neurol 1988;23(suppl):Sl13-S120
2. Mora CA, Garruto RM, Brown P, et al. Seroprevalence of antibodies to HTLV-Iin patients with chronic neurological disorders
other than tropical spastic paraparesis. Ann Neurol 1988;23
(supp1):S192-s 195
AIDS, Cytomegalovirus,
and the Brainstem
H. V. Vinters, M D
A recent letter to your journal [l] on the subject of cytomegalovirus encephalitis in a patient with acquired immunodeficiency syndrome (AIDS) presented views on neuropathology with which I do not agree. The author stated that
“CMV encephalitis presents in adults with AIDS as microglial nodules . . . and not-as multifocal necrotizing encephalitis.” The letter further made the claim that brainstem
lesions were unusual in individuals with AIDS and CMV
infection of brain.
In more than 30 cases of CMV encephalitis in the context
of AIDS examined at UCLA Medical Center, we have found
that involvement of the brainstem and especially the medulla
oblongata is common [2). We frequently found CMV inclusions and inflammation in the floor of the fourth ventricle in
the pons and medulla oblongata. In extreme cases, there was
also involvement by CMV of the cerebral aqueduct. In one
case, this was so severe that virtual occlusion of the cerebral
aqueduct had occurred because of periaqueductal CMV encephalitis and this had contributed to the development of a
noncommunicating hydrocephalus in an AIDS patient. In
addition, CMV can be found scattered focally along pial surfaces in the brainstem, just as it can be seen in a similar
location in the cerebral hemispheres. The well-known propensity of CMV to seed ependymal and subependymal surfaces has been carefully documented [3].
Caution must be exercised in ascribing structural abnormalities identified on computed tomographic scanning or
magnetic resonance image scanning to the presence of a
CMV encephalitis, or at least CMV encephalitis alone C2).
Again, in our experience CMV is frequently one of several
pathological processes occurring in the brains of AIDS pa-
Annals of Neurology Vol 25 No 3 March 1989 311
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narcolepsy, metabolites, reanalysis, fluid, monoamines, cerebrospinal
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