Epilepsy Behav. 2004
Dec;5(6):878-83. Levetiracetam for people with mental
retardation and refractory epilepsy.
Kelly K, Stephen LJ, Brodie MJ.
Epilepsy Unit, Division of Cardiovascular and Medical Sciences,
Western Infirmary, Glasgow G11 6NT, Scotland, UK.
Levetiracetam (LEV) is a novel antiepileptic drug (AED) with efficacy
against a wide range of seizures types. The aim of this observational
study was to assess its effectiveness in patients with mental retardation
and refractory epilepsy. Sixty-four patients were started on adjunctive
LEV after a 3-month baseline. LEV was initially dosed at 250 mg
daily and increased by 250 mg every 2 weeks thereafter according
to clinical response. Caregivers rated the patient's sleep, appetite,
alertness, and behavior as poor (1), reasonable (2), or good (3)
at each clinic visit. Patients were reviewed until one of four endpoints
was reached: seizure freedom for at least 6 months, > or = 50%
reduction in seizure frequency (responder) over a 6-month period,
<50% reduction in seizure frequency (marginal effect) over a
6-month period, or LEV withdrawal due to lack of efficacy, adverse
effects, or both. Twenty-four (38%) patients became seizure-free,
10 of whom were controlled on LEV 250 mg twice daily. An additional
18 (28%) patients were classified as responders, and 8 (12%) reported
only marginal benefit from adjunctive LEV. Fourteen (22%) patients
discontinued LEV (6 worsening seizures, 1 lack of efficacy, 7 adverse
effects). Caregivers rated combined sleep, appetite, alertness,
and behavior scores as "improved" at the end of follow-up
(P<0.001). LEV improved seizure control in the majority of patients
with mental retardation and may also have enhanced their quality
of life.
Thromb Res. 1995 Jun 15;78(6):469-82. The treatment of severe or recurrent deep
venous thrombosis. Beneficial effect of the co-administration
of antiplatelet agents with or without rheological effects, and
anticoagulants.
Moriau M, Lavenne-Pardonge E, Crasborn L, von Frenckell R, Col-Debeys
C.
Department of Internal Medicine, Haematology Division, Haemostasis
and Thrombosis Unit, University of Louvain (UCL), St.-Luc University
Clinics, Brussels, Belgium.
Deep venous thromboses can be divided into two groups according
to their pathogenesis, anatomical features and differing responses
to therapy. The first and most frequent consists of so-called
simple venous thrombosis while the second group, which is less
common, comprises severe or recurrent venous thrombosis characterised
by a multifactorial pathogenesis, a mixed thrombus rich in platelets
and by an incomplete response to both prophylactic and therapeutic
treatment with anticoagulants (heparin or vitamin K antagonist).
In a randomized, prospective blind study in patients with severe
or recurrent venous thrombosis, which included 6 groups each of
100 patients, co-administration of anticoagulants with various
types of antiplatelet agent, either with rheological effects (piracetam,
buflomedil, pentoxifylline) or without them (dipyridamole), has
shown a beneficial potentiating antithrombotic effect with those
drugs possessing rheological effects and the absence of this effect
with dipyridamole.
Int J Neuropsychopharmacol. 2004 Jul 1;:1-19.
Evidence-based pharmacotherapy of Alzheimers
disease.
Evans JG, Wilcock G, Birks J.
Cochrane Dementia and Cognitive Improvement Group, University of
Oxford, UK.
Dementia is an acquired global impairment of cognitive capacities.
Approximately 5% of people aged over 65 yr are affected by dementia,
and some 70% of cases are thought to be due primarily to Alzheimers
disease. Descriptions of the clinical manifestations of Alzheimers
disease have been increasingly refined in the last decade but there
is no diagnostic test for what remains fundamentally a pathologically
defined condition. At the present time interventions for Alzheimers
disease are limited to those that modify the manifestations of the
disease, and foremost amongst the candidates available are the cholinesterase
inhibitors. The rationale for the use of cholinergic drugs for Alzheimers
disease lies in enhancing the secretion of, or prolonging the half-life
of, acetylcholine in the brain. Several potential compounds have
been tested, but short half-lives and a high incidence of cholinergic
and other adverse effects have eliminated most. Only three are widely
licensed for use, donepezil, galantamine and rivastigmine. Their
efficacy is relatively modest. These drugs have been tested in 32
randomized, placebo-controlled trials. The trials assess cognitive
function primarily, and in addition they may assess global function,
activities of daily living, quality of life and behavioural disturbance
typically over 3 or 6 months. The performance of each drug is summarized
in a Cochrane review, a systematic review carried out according
to strict guidelines. There was a significant benefit in favour
of treatment compared with placebo for cognition and activities
of daily living, but withdrawals due to adverse events were significantly
higher for treatment than placebo for all three drugs. There is
little evidence from direct comparisons between the three drugs.
There are several economic analyses of the cost-effectiveness of
these drugs, but the findings cannot be considered robust owing
to inadequate data. A range of other pharmacological treatments
have been tested, including selegiline, piracetam, vitamin E, Ginkgo
biloba, anti-inflammatory drugs and hormone replacement therapy,
but, so far, Cochrane reviews have not established the efficacy
of these interventions for Alzheimers disease. A Cochrane review
of memantine shows benefits on cognitive and global function of
the same order of magnitude as seen for the cholinesterase inhibitors.
Memantine has been licensed in Europe for treatment of patients
with moderately severe to severe Alzheimers disease.
Br J Pharmacol. 2004 Jun;142(3):594-608. Piracetam and TRH analogues antagonise inhibition
by barbiturates, diazepam, melatonin and galanin of human erythrocyte
D-glucose transport.
Naftalin RJ, Cunningham P, Afzal-Ahmed I.
Physiology Division, Centre for Vascular Biology and Medicine,
Kings College London, Guys Campus, New Hunts House, London SE1
1UL.
1 Nootropic drugs increase glucose uptake into anaesthetised brain
and into Alzheimer's diseased brain. Thyrotropin-releasing hormone,
TRH, which has a chemical structure similar to nootropics increases
cerebellar uptake of glucose in murine rolling ataxia. This paper
shows that nootropic drugs like piracetam (2-oxo 1 pyrrolidine
acetamide) and levetiracetam and neuropeptides like TRH antagonise
the inhibition of glucose transport by barbiturates, diazepam,
melatonin and endogenous neuropeptide galanin in human erythrocytes
in vitro. 2 The potencies of nootropic drugs in opposing scopolamine-induced
memory loss correlate with their potencies in antagonising pentobarbital
inhibition of erythrocyte glucose transport in vitro (P<0.01).
Less potent nootropics, D-levetiracetam and D-pyroglutamate, have
higher antagonist Ki's against pentobarbital inhibition of glucose
transport than more potent L-stereoisomers (P<0.001). 3 Piracetam
and TRH have no direct effects on net glucose transport, but competitively
antagonise hypnotic drug inhibition of glucose transport. Other
nootropics, like aniracetam and levetiracetam, while antagonising
pentobarbital action, also inhibit glucose transport. Analeptics
like bemigride and methamphetamine are more potent inhibitors
of glucose transport than antagonists of hypnotic action on glucose
transport. 4 There are similarities between amino-acid sequences
in human glucose transport protein isoform 1 (GLUT1) and the benzodiazepine-binding
domains of GABAA (gamma amino butyric acid) receptor subunits.
Mapped on a 3D template of GLUT1, these homologies suggest that
the site of diazepam and piracetam interaction is a pocket outside
the central hydrophilic pore region. 5 Nootropic pyrrolidone antagonism
of hypnotic drug inhibition of glucose transport in vitro may
be an analogue of TRH antagonism of galanin-induced narcosis.
Pediatr Neurol. 2004 Apr;30(4):254-6.
Levetiracetam in the treatment of Lennox-Gastaut
syndrome.
De Los Reyes EC, Sharp GB, Williams JP, Hale SE.
University of Arkansas for Medical Sciences, Arkansas Childrens
Hospital, Little Rock, Arkansas, USA.
Lennox-Gastaut syndrome is an epileptic encephalopathy characterized
by multiple seizure types, mental retardation, and a slow spike-and-wave
pattern on electroencephalography. Medical intractability is common.
We identified a case series of six patients diagnosed with Lennox-Gastaut
syndrome in which levetiracetam was initiated as add-on therapy
for the management of seizures. At follow-up, four patients experienced
100% reduction of their myoclonic seizures; two patients had greater
than 50% reduction of their atonic seizures, and four patients
experienced 100% reduction in their generalized tonic-clonic seizures.
Tonic seizures were not responsive to treatment. The most common
side effect was irritability; the most positive change involved
alertness. In this small sample, levetiracetam appeared effective
in reducing seizures in Lennox-Gastaut syndrome. This preliminary
study is limited by its retrospective design and small number
of patients, but positive findings warrant a larger scale, multicenter
study.
Headache. 2004 Mar;44(3):238-43. Efficacy and safety of levetiracetam in
pediatric migraine.
Miller GS.
Pediatric Neurology Department, Hillcrest Healthcare System, Childrens
Medical Center, Tulsa, Okla. 74104, USA.
BACKGROUND: Headache is a frequent occurrence among children and
adolescents. Chronic headaches can be severe and disabling, and
require prophylactic treatment; however, additional data on the
use of prophylactic medications for migraine in children are needed.
OBJECTIVE: To review the efficacy and safety of levetiracetam
(Keppra) in pediatric patients with a history of recurrent headache.
DESIGN/METHODS: Data from 19 pediatric patients were retrospectively
reviewed. The initial dose of levetiracetam was usually 125 or
250 mg twice daily, but varied depending upon clinical judgment.
RESULTS: Charts of 9 girls and 10 boys (mean age, 11.9 years)
were reviewed. A variety of medications, including triptans, had
been used before initiating treatment with levetiracetam. Mean
headache frequency before treatment was 6.3 per month (standard
deviation [SD], 3.8; confidence interval [CI], 4.4 to 8.1). Duration
of headaches ranged from 0.25 to 8 years. Migraine (63.2%) and
migraine with aura (15.8%) were the most common types of headache
reported. Most patients (89.5%) had headaches that were severe.
After treatment, the mean headache frequency decreased to 1.7
per month (SD, 2.7; CI, 0.4 to 3.0), representing a reduction
compared with baseline (P <.0001). Levetiracetam eliminated
headaches in 10 patients (52.6%), and 7 patients (36.8%) had less
severe and less frequent headaches. Levetiracetam did not have
an effect on headaches in 2 patients (10.5%). Mean duration of
treatment with levetiracetam was 4.1 months. Doses ranged from
125 to 750 mg twice daily. Sixteen patients (84.2%) reported no
side effects on levetiracetam. One patient experienced asthenia/somnolence
and dizziness, and irritable, hyperactive, and hostile behavior
led to discontinuation of levetiracetam in another patient. A
third patient experienced irritability and moodiness that attenuated
after 1 month of treatment and did not require discontinuation.
CONCLUSIONS: In this small retrospective review, levetiracetam
was found to be generally well tolerated and appears to be a promising
candidate for additional evaluation in well-controlled clinical
trials of pediatric patients with migraine.
Dement Geriatr Cogn Disord 2002;13(4):217-24.
Clinical efficacy of piracetam in cognitive
impairment: a meta-analysis.
Waegemans T, Wilsher CR, Danniau A, Ferris SH, Kurz A, Winblad
B.
Research and Development, UCB SA (Pharma Sector), Braine-lAlleud,
Belgium.
A meta-analysis has been performed including nineteen double blind,
placebo controlled studies with piracetam in patients suffering
from dementia or cognitive impairment in the elderly. These studies
had as common outcome measure a clinical global impression of
change, a measure of clinically meaningful improvement. The meta-analysis
of this global outcome followed the methodology set forward by
the Cochrane Collaboration. This article describes the studies,
the patient populations and the methods of data extraction. The
results of the meta-analysis demonstrate a difference between
those individuals treated with piracetam and those given placebo,
both as significant odds ratio and as a favourable number needed
to treat. While there may be problems in meta-analyses and the
interpretation of the statistical results, the results of this
analysis provide compelling evidence for the global efficacy of
piracetam in a diverse group of older subjects with cognitive
impairment.
Cochrane Database Syst Rev. 2002;(4):CD000419.
Piracetam for acute ischaemic stroke.
Ricci S, Celani MG, Cantisani AT, Righetti E.
Stroke Service, USL 2, Via Guerra 17, 06127 Perugia, Italy.
BACKGROUND: Piracetam has neuroprotective and antithrombotic effects
which may help to reduce death and disability in people with acute
stroke. OBJECTIVES: The objective of this review was to assess
the effects of piracetam in acute presumed ischaemic stroke. SEARCH
STRATEGY: We searched the Cochrane Stroke Review Group Trials
Register (last searched April 2001). In addition we searched the
Cochrane Controlled Trials Register (Cochrane Library 2001, issue
2), MEDLINE (1966-April 2001), EMBASE (1980-April 2001), and ISI
Science Citation Index (1981- April 2001). We also handsearched
15 journals and contacted the manufacturer to identify further
published and unpublished studies. SELECTION CRITERIA: Randomised
trials comparing piracetam with control, with at least mortality
reported and entry to the trial within approximately 48 hours
of stroke onset. DATA COLLECTION AND ANALYSIS: Two reviewers extracted
data and assessed trial quality and this was checked by the other
two reviewers. Study authors were contacted for missing information.
MAIN RESULTS: Three trials involving 1002 people were included,
with one trial contributing 93% of the data. Participants' ages
ranged from 40 to 85, and both sexes were equally represented.
Piracetam was associated with a statistically non significant
increase in death at one month (approximately 31% increase, 95%
confidence interval 81% increase to 5% reduction). This trend
was no longer apparent in the large trial after correction for
imbalance in stroke severity. Limited data showed no difference
between the treatment and control groups for functional outcome,
dependency or proportion of patients dead or dependent. Adverse
effects were not reported. REVIEWER'S CONCLUSIONS: There is some
suggestion (but no statistically significant result) of an unfavourable
effect of piracetam on early death, but this may have been caused
by baseline differences in stroke severity in the trials. There
is not enough evidence to assess the effect of piracetam on dependency.
J ECT. 2002 Sep;18(3):130-7. Effect of piracetam on ECT-induced cognitive
disturbances: a randomized, placebo-controlled, double-blind study.
Tang WK, Ungvari GS, Leung HC.
Department of Psychiatry, Chinese University of Hong Kong, Hong
Kong, SAR, China.
Electroconvulsive therapy (ECT) is still the fastest, most effective,
and frequently life-saving therapeutic intervention in several
forms of depression and some other psychiatric disorders. Transient
memory disturbances are frequent after ECT. A randomized, double-blind,
placebo-controlled study was conducted to investigate the effects
of piracetam on ECT-induced confusion and memory disturbances.
Thirty-eight consecutively admitted patients with depressive illness
or schizophrenia requiring ECT were given either piracetam or
an identical-looking placebo during the period of ECT treatment
and for 2 weeks afterward. Daily dosage of piracetam was 7.2 g,
given orally for the first 2 weeks while patients underwent ECT
(loading phase), followed by 4.8 g for the rest of the study period.
Participants were evaluated by standardized clinical rating scales
and cognitive psychologic tests 1 to 2 days before ECT, 1 day
after their third and sixth ECT treatments, and 2 weeks after
they had completed their ECT courses. Piracetam had no significant
effect in preventing ECT-induced memory disturbances. All clinical
ratings were consistently, albeit not significantly, better in
the piracetam group, suggesting that piracetam may have augmented
the effects of ECT.
Cochrane Database Syst Rev. 2001;(2):CD001011.
Piracetam for dementia or cognitive impairment.
Flicker L, Grimley Evans G.
Royal Perth Hospital, University of Western Australia, Box X2213
GPO, Perth, WA, Australia, 6847.
OBJECTIVES: To determine the clinical efficacy of piracetam for
the features of dementia or cognitive impairment, classified according
to the major subtypes of dementia: vascular, Alzheimer's disease
or mixed vascular and Alzheimer's disease, or unclassified dementia,
or cognitive impairment not fulfilling the criteria for dementia.
SEARCH STRATEGY: The trials were identified from a search of the
Specialized Register of the Cochrane Dementia and Cognitive Improvement
Group on 10 November 2000 using the term spiracetam, nootropic
and 2-Oxo-1-pyrrolidine. In addition the pharmaceutical company
responsible for marketing most of the piracetam worldwide, UCB
Pharma, provided a comprehensive list of abstracts, which included
many unpublished studies. As many of these unpublished, placebo-controlled
studies will be reviewed as possible. SELECTION CRITERIA: All
unconfounded trials specified as randomized in which treatment
with piracetam was administered for more than a day and compared
with placebo in patients with dementia of Alzheimer type, vascular
dementia,or mixed vascular and Alzheimer's disease, or unclassified
dementia, or cognitive impairment not fulfilling the criteria
for dementia. DATA COLLECTION AND ANALYSIS: Data were extracted
independently by two reviewers. Each study was independently verified
as fulfilling the inclusion criteria. Studies were rated for methodological
quality by assessment of blinding and loss before analysis as
described by Jadad et al. (1996). Studies were pooled if appropriate
and possible, and the pooled odds ratios (95%CI) or the average
differences (95%CI) were estimated. Where possible, intention-to-treat
analyses were undertaken. Sensitivity analyses were performed
to determine if successive elimination of those studies performing
most poorly on these quality criteria changed the effect estimate.
MAIN RESULTS: Unfortunately, many of the studies were of cross-over
design and first-phase data were unavailable, or could not be
extracted. Global Impression of Change was the only outcoeme for
which there was a significant volume of evidence from the pooled
data. There was evidence of heterogeneity in the results from
the individual studies, chi-square test = 20.8 (df=5). Using a
fixed effects model the odds ratio for improvement in the piracetam
group compared with the placebo group was 3.55, [95% CI][2.45,
5.16]. If a random effects model was used the odds ratio was 3.47
[1.29, 9.30]. If one single-blind study was excluded, the fixed
effects model yielded an odds ratio of 3.36 [2.29, 4.99] and if
a random effects model was applied then the odds ratio was 2.89
[1.01, 8.24]. The evidence of effects on cognition and other measures,
was inconclusive. REVIEWER'S CONCLUSIONS: At this stage the evidence
available from the published literature does not support the use
of piracetam in the treatment of people with dementia or cognitive
impairment. Although effects were found on global impression of
change, no benefit was shown by any of the more specific measures.
There is a need for further evaluation of piracetam by : 1) Obtaining
the data from the identified studies for an individual patient
database review, 2) Performing a randomized trial of piracetam
in patients with diagnoses made by currently accepted diagnostic
criteria. The trial should extend over for a period of at least
6 months and preferably longer. Specific cognitive instruments
which are sensitive to change, Clinician Global Impression of
Change, levels of dependency and caregiver quality of life scales
should also be incorporated in such a study.
Stroke. 2000 Sep;31(9):2112-6. Piracetam improves activated blood flow
and facilitates rehabilitation of poststroke aphasic patients.
Kessler J, Thiel A, Karbe H, Heiss WD.
Max-Planck-Institute for Neurological Research, Cologne, Germany.
BACKGROUND AND PURPOSE: In a prospective, double-blind, placebo-controlled
study, it was investigated whether piracetam improves language
recovery in poststroke aphasia assessed by neuropsychological
tests and activation PET measurement of cerebral blood flow. METHODS:
Twenty-four stroke patients with aphasia were randomly allocated
to 2 groups: 12 patients received 2400 mg piracetam twice daily,
12 placebo. Before and at the end of the 6-week treatment period
in which both groups received intensive speech therapy, the patients
were examined neuropsychologically and studied with H(2)(15)O
PET at rest and during activation with a word-repetition task.
Blood flow was analyzed in 14 language-activated brain regions
defined on reconstructed surface views from MRI coregistered to
the PET images. RESULTS: Before treatment, both groups were comparable
with respect to performance in language tasks and to type and
severity of aphasia. In the piracetam group, increase of activation
effect was significantly higher (P:<0.05) in the left transverse
temporal gyrus, left triangular part of inferior frontal gyrus,
and left posterior superior temporal gyrus after the treatment
period compared with the initial measures. The placebo group showed
an increase of activation effect only in the left vocalization
area. In the test battery, the piracetam group improved in 6 language
functions, the placebo group only in 3 subtests. CONCLUSIONS:
Piracetam as an adjuvant to speech therapy improves recovery of
various language functions, and this effect is accompanied by
a significant increase of task-related flow activation in eloquent
areas of the left hemisphere.
Orv Hetil. 2000 May 28;141(22):1189-93. Cognitive enhancement effect of piracetam
in patients with mild cognitive impairment and dementia.
Tariska P, Paksy A.
Memoria Klinika, Orszagos Pszichiatriai es Neurologiai Intezet,
Budapest.
Effectiveness and tolerability of two piracetam-containing drugs
were compared in the frame of an open, multicentre, Phase-IV,
prospective study with group and self control carried out in 9
Hungarian centres in 1998. Patients with cognitive decline from
Alzheimer's disease and/or cerebrovascular origin have received
the drug, in the first 4 weeks in 4800, later 2400 mg daily doses.
One hundred four patients finished the study. No relevant difference
with statistically significant degree was registered between the
two groups. Based on this fact in this study data of the 104 patients
were examined together. Authors examined two problems. The first:
on which cognitive function is more effective the drug. Five factors
of the modified Mini-Mental State Examination were separated and
compared. Nearly all of them significantly increased especially
the factors of memory, and concentration-psychomotor speed. The
second examined field: are there certain subgroups with prognostic
value about the effectiveness of piracetam treatment. Neither
the duration of the illness, nor etiologic diagnosis, severity
of cognitive decline, or former treatment with piracetam did influence
significantly the efficacy. In case of depressive symptoms such
connection was established: the more pronounced the severity of
these symptoms the higher improvement can be expected in cognitive
functions. This was also stressed by the logistic regression analysis.
Authors described an original evaluation method of the trail-making
test, which could widen the application of this popular test in
psychopharmacologic studies. Final conclusions: the cognitive
enhancer effect of piracetam appeared in a few weeks. This treatment
could be effective even in Alzheimer's disease, in case of more
pronounced cognitive decline, longer duration of the illness,
and in case of former piracetam treatment as well. The degree
of cognitive improvement was most pronounced in patients with
comorbid depressive symptoms.
J Neural Transm. 1999;106(7-8):757-61. Piracetam reverses hippocampal membrane
alterations in Alzheimers disease.
Eckert GP, Cairns NJ, Muller WE.
Department of Pharmacology, Biocenter, University of Frankfurt,
Federal Republic of Germany.
The in vitro effects of piracetam treatment on the fluidity of
membranes from the hippocampus of Alzheimer's Disease patients
(AD) and non-demented controls were studied. Hippocampal membranes
of AD patients showed a significant lower hydrocarbon core fluidity
compared with membranes from elderly non-demented controls. Preincubation
with piracetam enhanced the hydrocarbon core fluidity of hippocampal
membranes from AD-patients as well as elderly controls in a concentration
depending fashion, although the effect was more pronounced for
the AD membranes. In the presence of piracetam, the difference
of the membrane fluidity between AD and control membranes was
not longer apparent.
J Clin Pharm Ther. 1999 Oct;24(5):369-74. Piracetam in the treatment of schizophrenia:
implications for the glutamate hypothesis of schizophrenia.
Noorbala AA, Akhondzadeh S, Davari-Ashtiani R, Amini-Nooshabadi
H.
Roozbeh Psychiatric Hospital, Tehran University of Medical Sciences,
Tehran, Iran.
OBJECTIVE: There is a growing interest in investigating the role
of glutamate receptors in the pathophysiology of schizophrenia.
Indeed, the hyperdopaminergic theory of schizophrenia can explain
only the positive symptoms of schizophrenia, whereas the glutamate
hypothesis may provide a more comprehensive view of the illness.
We undertook a trial to investigate whether the combination of
haloperidol with piracetam, a nootropic agent which modulates
the glutamate receptor positively was more effective than haloperidol
alone. METHODS: Thirty patients who met the DSM IV criteria for
schizophrenia completed the study. Patients were allocated in
a random fashion, 14 to haloperidol 30 mg/day plus piracetam 3200
mg/day and 16 to haloperidol 30 mg/day plus placebo. RESULTS:
Although both protocols significantly decreased the score of the
positive symptoms, the negative symptoms, the general psychopathological
symptoms and the total score of PANSS scale over the trial period,
the combination of haloperidol and piracetam showed a significant
superiority over haloperidol alone in the treatment of schizophrenic
patients. CONCLUSION: Piracetam, a member of the nootropic class
of drugs and a positive modulator of glutamate receptor, may be
of therapeutic benefit in treating schizophrenic patients in combination
with typical neuroleptics. However, a larger study to confirm
our results is warranted.
Zh Nevrol Psikhiatr Im S S Korsakova. 1997;97(10):29-34.
Nootropil in the treatment of disorders
of the higher mental functions in patients with an ischemic stroke.
Burd GS, Gekht AB, Bogolepova AN, Buklina SB.
47 patients with acute ischemic stroke were treated with nootropil
(pyracetam, UCB, Belgium) from the first day of the disease (12
g, intravenously, by drops during 2 weeks, then 4.8 g, per os)
on the background of basic therapy. There was revealed increase
of spontaneous activity, expressive and impulsive speech, audio-
and speaking memory (especially delayed memory), tactile, acoustic
and visual gnosis, space praxis. There was observed more pronounced
positive dynamics of functions of damaged hemisphere in patients
with localisation of ischemic focus in left hemisphere. Meanwhile
restoration was slower when ischemic focus was localized in right
hemisphere. Restoration of high mental functions occurred to be
faster during nootropil treatment as compared with basic therapy
only. The conclusion was made that nootropil can be prescribed
for the patients with hemispheric ischemic stroke and especially
for the patients with alterations of cerebral circulation in system
of internal carotid artery including such disturbances on the
background of insufficiency of circulation in vertebrobasilar
system.
Klin Med (Mosk). 1989 May;67(5):36-8. Experience using nootropil in patients
with chronic ischemic heart disease.
Shubina TI, Zaitsev VP.
Course nootropil treatment was conducted in 34 IHD patients with
neurotic and neurotic-like diseases. Dynamic changes in the psychic
state were assessed by the clinical scale and the MMPI psychological
test. Significant improvement or normalization of the psychic
state was achieved in 58.8 per cent of the patients treated with
nootropil. The best results were obtained in the treatment of
asthenic states. Administration of nootropil had no influence
on the incidence of angina pectoris attacks and produced no side
effects.
