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Cocaine and tourette's syndrome.

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trihexyphenidyl is the drug of first choice for dystonia [I),
the history of parotid abscess mitigated against the use of a
drug that would cause dry mouth. Therapy with bethanechol,
5 to 10 mg three times a day, allowed dosage with uihexyphenidyl up to 40 mg per day with 95% improvement in
the patient’s symptoms, including resumption of driving.
The use of bethanechol, 5 to 10 mg three or four times a
day titrated by the patient to diminish dry mouth but avoid
gastrointestinal cramping, has since been helpful in several
other patients, including elderly ones. Although the use of
muscarinic agonists per se is contraindicated in patients with
asthma, coronary artery disease, and peptic ulcer disease,
bethanechol could be well tolerated in such patients when it
is used solely to diminish the side effects of concurrently
administered anticholinergic agents.
University of Colorado Health Sciences Center
Denver, CO
SSPE (n = 3)
Controls (n = 6)
Chemotactic Index*
5 SD
*The chemotactic index (CI) was calculated by the following formula:
Number of PMN in 10 random fields
CI =
Number of PMN ( X lo6) in 0.4 ml delivered
to starting side of filter
?Percentage of Escherichia coli killed at 60 minutes.
SSPE = subacute sclerosing panencephalitis; PMN = polymorphonuclear leukocyte.
*Departmentof Pediatrics
TDepartment of Neurology
University of Catania
Catania, Italy
Fahn S . Hgh dosage anticholinergictherapy in dystonia. Neurology 1983;33:1255-1261
Leukocyte Function
in Subacute Sclerosing
Nunzia Atzia, MD,* Agata Sciacca, MD,#
Davide Maimone, MD,t and Luigi M. E. Grimaldi, MDt
In 1976, Anderson and colleagues 11) found transient decreased random migration and chemotactic ability of polymorphonuclear leukocytes (PMNs) in children with measles.
Normal PMN motility was observed by the eleventh day
after the onset of rash. They suggested that this defective
motility could be due to intrinsic cell abnormalities because
endotoxin-activated sera from these patients generated normal chemotactic activity.
Recently we evaluated PMN motility and bactericidal activity in 3 children with subacute sclerosing panencephalitis
(SSPE). Their ages ranged from 8 to 10 years and all were in
the second stage of the disease, onset having occurred 13 to
24 months before study. Random migration and chemotactic
ability of their PMNs were determined by modified Boyden
chamber technique according to Ferrari’s method 12). Bactericidal capacity was assayed by the method of Quie and
colleagues f3). The chemotactic index demonstrated that
PMN motility was within normal range in the patients with
SSPE as compared with healthy children (Table). No difference was seen in the bactericidal activity. In cases of acute
measles antigens have been detected in both PMN leukocytes and lymphocytic cells 147, while in SSPE the virus
RNA sequences have been demonstrated only in lymphocytes and neural tissue 15). Furthermore, pyogenic infections
in SSPE are not as frequent as in acute measles.
The data show normal PMN function in our patients and
suggest a lack of involvement of these cells in SSPE.
1. Anderson R, Rabson AR,et al. Defective neutrophil motility in
children with measles. J Pediav 1976;89:27-32
2. Ferrari F, Marconi M, Notarangelo LD, er al. Funzionaliti
granulocitaria Boll Assoc Ematol Oncol Pediau 1985;14:89-95
3. Quie PG, White G, Holmes B, Good RA. In vitro bactericidal
capacity of human polymorphonuclearleukocytes: diminished activity in chronic granulomatous disease of childhood. J Clin Invest 1967;46:668-679
4. Joseph BS, Marnper PM, Oldstone MA. Replication and persistence of measles virus in defined subpopulations of human leukocytes. J Virol 1975;16:1638-1648
5. Foumier JG, Tardieu M, Lebon P, et al. Detection of measles
virus RNA in lymphocytes from peripheral blood and brain
perivascular infiltrates of patients with subacute sclerosing
panencephalitis. N Engl J Med 1985;313:910-915
Locame and
Tourette’s Syndrome
Stewart A. Factor, DO,
Juan R. Sanchez-Ramos, MD, PhD,
and William J. Weiner, MD
A 2 I-year-old man experienced cocaine-induced exacerbations of symptoms previously diagnosed as Tourette’s syndrome (TS). Symptoms began at age 10 with uncontrollable
eye blinking and head twitching. The tics waxed and waned
and varied in anatomic distribution. Within 2 years vocal tics
consisting of grunting and short high-pitched sounds began.
Haloperidol and pimotide were helpful but were discontinued because of adverse effects, including anxiety and involuntary mouth closure. The patient reported that within 20
minutes of self-adminisuation of cocaine via the nasal route,
the frequency and amplitude of motor and vocal tics increased, corresponding with development of euphoria Increased motor and vocal symptoms lasted 1 to 2 hours before eventually returning to baseline. Similar, but less severe,
exacerbations appeared each time he used cocaine but not
after marijuana or alcohol use. On neurological examination
the patient had motor tics involving the head and neck and
Annals of Neurology Vol 23 N o 4 April 1988 423
vocal tics consisting of grunting and high-pitched sounds.
The rest of the examination was normal.
This is the second reported case of cocaine-induced exacerbation of TS El]. In both cases a diagnosis of TS was
established prior to the use of cocaine. Exacerbations closely
followed cocaine administration and reversed within hours.
The pathogenesis and neurochemistry of TS are unknown.
A key role for the dopaminergic system in the clinical manifestations of this syndrome has been postulated. This hypothesis is based on indirect evidence which includes the
efficacy of the dopamine antagonists haloperidol and
pimozide in TS, the occurrence of TS after long-term treatment with neuroleptics (tardive Tourette’s) [ 2 } , and the results of neurochemical studies of catecholamine metabolites
in the CSF which demonstrate low levels of homovanillic
acid in untreated TS patients 131. Cocaine inhibits the reuptake of dopamine and norepinephrine. Inhibition of dopamine uptake governs self-administration responses and reinforcement in laboratory animals and abuse in humans 141.
Effects related to abuse include feelings of well-being and
euphoria. Since exacerbations of TS occurred during the
euphoric state it is likely that dopamine uptake inhibition
played a role in both. In addition, tricyclic antidepressant
medications are potent inhibitors of the reuptake of nor-
424 Annals of Neurology Vol 23 No 4 April 1988
epinephrine; however, they are also weak inhibitors of
dopamine reuptake and do not exacerbate TS. Therefore,
the effect cocaine has on dopaminergic transmission is likely
to be responsible for the alterations in the manifestations of
TS. The exacerbation of TS by cocaine supports the hypothesis that TS may be the result of altered central
dopaminergic mechanisms.
Uniuersity of M i a m i
School of Medicine
Department of Neurology
Miami, FL
1. Mesulam MM. Cocaine and Tourette’s syndrome (letter). N Engl
J Med 1986;315:398
2. Klawans HL, Falk DK, Nausieda PA, Weiner WJ. Gilles de la
Tourette syndrome after long term chlorpromazine therapy.
Neurology 1978;28:1064-1068
3. Butler IJ, Koslow SH, Seifert WE, et al. Biogenic amine metabolism in Tourette syndrome. Ann Neurol 1979;6:37-39
4. Rim MC, Lamb RJ, Goldberg SR, Kuhar MJ. Cocaine receptors
on dopamine transporters are related to self administration of
cocaine. Science 1987;237: 12 19- 1223
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syndrome, tourettes, cocaine
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