04 01

BOLETIN LATINOAMERICANO Y DEL
CARIBE DE PLANTAS MEDICINALES Y

AROMATICAS
Publicacin Electrnica Bimestral Registrada en LATINDEX
!SSN 0717 7917
Enero de 2005; Volumen 4: Nmero 1

"Desde el Ro Grande a la Patagonia,
incluyendo el Caribe de habla Espaola, Inglesa y Francesa"

Editores
Jefe: Jos L. Martnez (Chile)
Asociado: Jorge Rodrguez (Cuba)
Ejecutivo: Jos M. Prieto (Espaa)

Supervisores de Edicin
Patricia Landzuri (Colombia)
Gabino Garrido (Cuba)

Co-editores
Arnaldo Bandoni (Argentina)
Maria E. Medina (Nicaragua)
Francisco Morn (Cuba)
Patrick Moyna (Uruguay)

Presidente de la SLF (2002 -2005)
Virginia Martino (Argentina)

Bajo el auspicio de la

Sociedad Latinoamericana de Fitoqumica

Consejo Editorial
Christian Agyare (Ghana)
Jorge Alonso (Argentina)
Pastor Arenas (Argentina)
Elizabeth Barrera (Chile)
Henry Y. Bernal (Colombia)
Armando Cceres (Guatemala)
Bruce Cassels (Chile)
Geoffrey Cordell (EUA)
Marco Dehesa (Ecuador)
Carla Delporte (Chile)
Pilar DOcn (Espaa)
Luis Doreste (Venezuela)
Angela Duque (Colombia)
Norman R. Farnsworth (EUA)
Mildred Garca (Costa Rica)
Martha Gatusso (Argentina)
Mahabir Gupta (Panam)
Alberto Hernndez (Cuba)
Peter Houghton (Reino Unido)
Ana Ladio (Argentina)
Ingrid Loayza (Bolivia)
Olga Lock (Per)
Vicente Martnez (Guatemala)
Ernesto Medina (Nicaragua)
Pedro Melillo de Magalhaes (Brasil)
Jordi Molg (Francia)
Miguel Morales (Chile)
John A. O. Ojewole (Sudfrica)
Mahendra Rai (India)
Rosala Ramrez (Mxico)
Elsa Rengifo (Per)
Alicia Rodrguez (Cuba)
Carles Roersch (Repblica Dominicana)
Marcela Samarotto (Chile)
Aurelio San Martin (Chile)
Jos San Martn (Chile)
Marco Schwartz (Chile)
Nikolai Sharapin (Brasil)
Mario Silva (Chile)
Djaja D. Soejarto (EUA)
Mauricio Venegas (Chile)
Carlos Vicente (Argentina)
Roger Villalobos (Costa Rica)
Rita Zeichen (Argentina)
Xing Zu Zhu (Repblica Popular China)
Gustavo Ziga (Chile)
B
B
L
L
A
A
C
C
P
P
N
N
A
A

BLACPMA.- Enero de 2005; Volumen 4, N 1, p. 2

Objetivos del Boletn
ndice

Estimular a los grupos de trabajo existentes
en Latinoamrica, sean investigadores,
productores, funcionarios o simplemente
interesados en las plantas medicinales y
aromticas, poniendo a su disposicin
este Boletn para la difusin y la
divulgacin de sus investigaciones y de
las actividades que en general desarrollen
en torno a plantas.

Ser una herramienta de difusin para la
Sociedad Latinoamericana de Fitoqumica
principalmente y de otras sociedades y
agrupaciones que se sientan
representadas por este Boletn.

Constituir un nexo entre los profesionales
de habla hispana, francesa, portuguesa e
inglesa de la regin, relacionados con el
tema central del Boletn

Nota Editorial J Editorial............ 3
Artculo Original................ 4
Indigenous remedies and epilepsy:
evaluation of some South-African
medicinal plants used as anticonvulsivant
remedies in Zulu folk medicine

John A. O. Ojewole

Correspondencia................ 20

www.blacpma.cl

Instrucciones para los Autores
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MEDICINALES Y AROMTICAS {BLACPMA), es una publicacin
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Los trabajos se dividiran en !ntroduccin, Nateriales y Ntodos,
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autores, institucin a la cual pertenecen los autores, direccin del
autor principal y correo electrnico. Debera aparecer ademas un
resumen en espanol e ingls de no mas de 100 palabras, un titulo
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las figuras deben ser arabigos.
Las referencias bibliograficas se numeraran segun el orden de mencin
en el texto y deberan identificarse con numero arabigos. Se incluiran
citas de documentos relevantes y publicados; los documentos no
publicados o citas personales se incluiran dentro del texto entre
parntesis. A continuacin algunos ejemplos de los principales
casos:
Revistas:
Kostennikova ZA. (1983). Uv spectrophotometric quantitative
determination of flavonoids in Calendula tincture. Farmatsiya 33 (6):
83 - 8
Soto H, Rovirosa J, San Nartin A, Argandona v. (199+). Netabolitos
secundarios de Dictyota crenulata. Bol. Soc. Chil. Quim.39 (3): 173-
178.
Libros
Durand E, Niranda N, Cuellar A. (1986). Nanual de practicas de
laboratorio de Farmacognosia. Ed. Pueblo y Educacin, La Habana,
Cuba 130 pp.
Captulos de Libros:
Lopes de Almeida JN. (2000). Formulacin farmacutica de
productos fitoteraputicos, pp 113-12+. En Sharapin, N:
Fundamentos de tecnologia de productos fitoteraputicos. Ed. CAB y
CYTED, Bogota, Colombia.
Gracias de antemano por sus colaboraciones

Nota Editorial

Editorial
Estimados amigos:
!niciamos un nuevo ano de vida de BLACPMA, aunque si
bien su cumpleanos es en el mes de Nayo. Como
pueden ver con nueva imagen que esperamos sea de su
agrado, todo esto gracias al gentil apoyo del Dr. Jos
Naria Prieto de Espana.
En esta nueva etapa, cada autor que publique un articulo
recibiran en forma attacheada un ejemplar de su
articulo con una novedosa forma la cual tambin sera
incluida en algunas bases de datos para que ademas de
BLACPMA sean conocidas sus obras en el mundo
liberal.
Quiero hacer un parntesis por una situacin planteada
durante el ano anterior, quiero tomar un trozo textual
de una nota enviada a mi por el Dr. Francisco Norn, de
La Habana, Cuba y Co-Editor de BLACPMA luego de
hacer la consulta a todos los co-editores para aclarar un
concepto fundamental en este tipo de publicaciones:
.por definicin de "autor" esta implicito que son los
que aparecen en una publicacin y que participaron
activamente en el diseno, ejecucin (al menos de una
parte), discusin de los resultados y elaboracin del
articulo. El que solo hizo una parte NO es autor, se pone
en agradecimiento y se senala lo que hizo. El primer
autor es el de mayor participacin en la investigacin y
por consiguiente en el articulo. Es usualmente el que
aport la idea. NO es procedente poner notas
aclaratorias en la revista al respecto. El autor principal
tiene la maxima responsabilidad".
Esta nota surge debido a que un co-autor de un articulo
nos envi una nota solicitando explicaciones respecto a
que su nombre aparecia en un articulo que l no
compartia. En ese sentido BLACPMA, sus editores y el
Comit Editorial son ajenos en lo que respecta a los co-
autores de un articulo quedando toda la responsabilidad
en el autor con el que nosotros mantenemos
correspondencia y que es quien nos ha enviado el
respectivo articulo.
Saludar al Prof. W.D. Ratnasooriya de Sri Lanka quien
pese a todos los problemas se encuentra bien junto a su
familia, dias despus del Tsunami recibi su nota: Dear
Dr. Nartinez, Thank you very much for your inquiring
about me and my family. ! greately appreciate your
gesture. We are safe. l ha publicado en BLACPMA y
tiene un articulo aceptado.
Jos Luis Martinez
Editor Jefe
Estimados amigos lectores,
Recin llegado a BLACPMA, tengo la satisfaccin de dirigirme a vds
para presentarles un nuevo numero de nuestro boletin. Su editor,
Jos Luis Nartinez, me ha honrado al aceptarme en su equipo de
trabajo y espero corresponder en todo lo posible a su gesto. Lo
que me impuls a contribuir a esta publicacin fu un doble
convencimiento: el de que BLACPMA era un proyecto consolidado
y el que una nueva esttica mas elaborada ayudaria, si cabe, a
llamar la atencin de un mayor numero de lectores.
Si bien este boletin naci con su punto de mira en el ambito
Latinoamericano, la procedencia de los trabajos y colaboraciones
recibidas ultimamente sobrepasan ampliamente su ambito
geografico originario. Ya en este numero el Dr. Ojewole nos habla
desde Sudafrica sobre las potencialidades de la medicina popular
zulu, mientras que en manos de nuestro Consejo Editorial obran
similares contribuciones llegadas de Africa, Asia y Norteamrica,
junto a otras habituales provenientes de Latinoamrica. Todo ello
es resultado de la credibilidad alcanzada por BLACPMA gracias al
trabajo de su equipo editorial desde el comienzo de su andadura.
BLACPMA cambia imagen para cumplir mejor su intencin: el de
ser un medio agil de difusin de informacin sobre Plantas
Nedicinales y Aromaticas, un foro de discusin abierto, y, por qu
no, una especie de carta que simplemente quiere recordarles cada
dos meses que Latinoamrica se mueve, y que cuando lo hace con
determinacin es capaz de mover con ella al mundo entero.
Esta ilusin por la renovacin de nuestro proyecto editorial se ve
empanada a ultima hora por la terrible catastrofe ocurrida en el
Sudeste Asiatico, donde BLACPMA cuenta con buenos amigos y
colaboradores, los cuales nos han informado que afortunadamente
estan sanos y salvos. La magnitud de la tragedia es inimaginable y
desde aqui aprovecho para mandar en nombre del Comit
Editorial un mensaje de esperanza y solidaridad para los
cientos de miles de damnificados.
Gracias por su fidelidad y apoyo. Son vds, los lectores, los jueces
ultimos de todo, y por ello les animamos a opinar y contribuir con
sus ideas y trabajos a sta que es su publicacin. Queremos llegar
hasta donde vds quieran que lleguemos.

Jos Mara Prieto
Editor Ejecutivo

Reciban un sincero deseo de
Feliz Ao Nuevo 2005
El Comit Editorial

Sudfrica
Artculo Original
INDIGENOUS REMEDIES AND EPILEPSY: EVALUATION OF SOME SOUTH
AFRICAN MEDICINAL PLANTS USED AS ANTICONVULSANT REMEDIES IN ZULU
FOLK MEDICINE
(Remedios indgenas y epilepsia: evaluacin de algunas plantas medicinales sudafricanas usadas como
anticonvulsivantes en medicina popular zul)

JOHN A. O. OJEWOLE

Department of Pharmacology, Faculty of Health Sciences, University of Durban-Westville.
Private Bag X54001, Durban 4000, South Africa.
Telephone: +27-31-260-7356; Fax: +27-31-260-7907; E-Mail: ojewole@pixie.udw.ac.za
Received: October 1, 2003; With Correction: February 20, 2004, Accepted June 10, 2004

Abstract

The work presented in this article reviews the current status of epilepsy and presents
preliminary findings of a recent anticonvulsant screening programme carried out on some
South African medicinal plants used as anticonvulsant remedies in Zulu folk medicine.
Current estimates suggest that approximately 6% of the worlds population suffer from
epilepsy. Life expectancy may be drastically reduced by this crippling disorder, especially
in developing countries of the world where its prevalence is increasing steadily, and
adequate treatment is often expensive or unavailable. In many developing countries of the
world, millions of people still rely on traditional healers and medicinal plants for their daily
primary health-care needs, and plant products are now gaining popularity as alternative
and complementary therapies even in industrialized, Western countries. Growing interests
in herbal medicine have prompted in-depth studies on the properties and uses of
medicinal plant materials, and raised concerns about their safety, efficacy and quality. In
many developing countries of the world, scientifically sound data are lacking for many
plant materials, extracts and active ingredients. The overall aim of this study is to provide
a starting point for African programmes leading to the development of indigenous plants
as inexpensive sources of effective, standardized crude antiepileptic drugs, and for the
discovery of lead compounds for new, safe and cheap anticonvulsant drug development.
This study was undertaken to examine the anticonvulsant effects of some South African
indigenous plants used as antiepileptic remedies in Zulu folk medicine. A total of 35
medicinal plants commonly used in Zulu traditional medicine as antiepileptic remedies
were collated, reviewed, collected, authenticated and screened pharmacologically for
anticonvulsant properties. Pharmacological examination of the 35 plants showed that their
aqueous extracts contain chemical compounds with weak to strong anticonvulsant
properties. Compared with phenobarbitone- or diazepam-treated test, and distilled water-
treated control mice, the magnitude of the anticonvulsant effects produced by each of the
aqueous plant extracts varied widely. Except in 2 out of the 35 cases, the plant extracts
were generally more effective in protecting the animals used in this study against
pentylenetetrazol (i. e., metrazol)-induced seizures than in protecting the mice against
picrotoxin-induced seizures. Of the 35 different plant extracts examined, 17 (i. e., 48.57%)
produced moderate to strong anticonvulsant effects in metrazol-induced, chemoshock
seizures (producing 62.50% 87.50% protections against metrazol-induced seizures in
the mice). The remaining 18 of the 35 (i. e., 51.43%) plant extracts showed weak to mild
anticonvulsant activities (producing 12.50% 50.00% protections against metrazol-
induced seizures in the animals). Maximal anticonvulsant effects of the plant extracts were
elicited at doses 800 mg/kg i. p., 15 30 minutes post administration. Compared with
the distilled water-treated control mice, phenobarbitone and diazepam produced very
strong and pronounced anticonvulsant effects in the mice. Although the anticonvulsant
actions of some of the plant extracts may have involved extra-GABAergic mechanisms, it
is likely that most of the plant extracts might have stimulated GABAA-receptors to produce
their anticonvulsant effects. Nevertheless, the results of this experimental animal study
have shown that the medicinal plant extracts examined possess weak to strong
anticonvulsant properties, and thus lend credence to the folkloric use of the plants as
antiepileptic remedies in Zulu traditional medicine.

Resumen

El trabajo presentado en este articulo revisa el estado actual de la epilepsia y presenta los
estudios preliminares de un programa reciente de cribado de anticonvulsivantes llevados a
cabo sobre plantas medicinales de Sudfrica usadas en la medicina folclrica zul.
Estimaciones recientes sugieren que el 6% de la poblacin mundial sufre de epilepsia. La
expectativa de vida se ve reducida drsticamente por este desorden invalidante,
especialmente en pases en va de desarrollo, en los cuales su prevalencia se va
incrementando paulatinamente, siendo los tratamientos muy costosos y a veces inaccesibles
para la poblacin. Por ello, en estos pases, millones de personas son tratadas diariamente
por mdicos no tradicionales con plantas medicinales, para la atencin primaria de su salud.
Los productos herbarios estn ganando popularidad como terapia alternativa o
complementaria tambin en pases occidentales industrializados. Este creciente inters en la
medicina herbaria ha promovido estudios mas profundos, relacionados con sus propiedades,
usos, seguridad, eficacia y calidad. Aun en pases desarrolados no existen datos cientficos
de las propiedades de las drogas crudas, sus preparaciones, e ingredientes activos. El
objetivo de este estudio es proveer un punto de inicio para programas africanos que
colaboren con el desarrollo de plantas indgenas como fuente econmica y estandarizada de
drogas crudas antiepilpticas, y asimismo con el descubrimiento de nuevas drogas, inocuas,
efectivas y econmicas para el tratamiento de esta patologa. Este estudio fue llevado a
cabo para examinar los efectos anticonvulsivantes de algunas plantas indgenas
sudafricanas utilizadas como remedios antiepilpticos en la medicina folclrica zul. Un total
de 35 plantas medicinales utilizadas en la medicina folclrica zul como anticonvulsivantes
fueron escogidas, coleccionadas, autentificadas y sometidas a cribado farmacolgico para
probar sus propiedades anticonvulsivantes. La observacin farmacolgica de los 35
extractos acuosos, mostraron que los mismos contenan compuestos qumicos con suave a
fuerte propiedad anticonvulsivante. Fueron comparadas con fenobarbital o diazepam
(referencias) y agua destilada (control), en ratones. Las magnitudes de las propiedades
anticonvulsivantes producidas por cada extracto acuoso, mostraron una amplia variacin.
Con excepcin de 2, los extractos fueron mas efectivos en la proteccin de animales
tratados con pentilenetetrazol. De los 35 diferentes extractos acuosos examinados, 17
(48,57%) provocaron moderados a fuertes efectos anticonvulsivantes, en la reversin de las
convulsiones inducidas por metrazol. Los restantes 18 extractos (51,43%) mostraron dbil a
suave actividad anticonvulsivante, 12,50%-50% de proteccin contra el metrazol. Los
mayores efectos logrados, fueron con dosis mayor o igual a 800 mg/kg i.p., 15 minutos luego
de la administracin. Comparados con el agua destilada, el fenobarbital y el diazepam,
produjeron una fuerte y pronunciada actividad anticonvulsivante en ratones. Aunque las
acciones anticonvulsivantes de algunos extractos pueden haber involucrada mecanismos
GABArgicos, es probable que la mayora de los extractos vegetales, puedan haber
estimulado receptores GABA A, para producir su efecto anticonvulsivante. Los resultados de
este estudio experimental en animales han mostrado que los extractos medicinales
examinados poseen de suaves a fuertes propiedades anticonvulsivantes, avalando as el
uso folclrico de las plantas, como remedios antiepilpticos en la medicina tradicional zul.

Key words: Traditional Medicine; South African Medicinal Plants; Epilepsy;
Indigenous Anticonvulsant Remedies; Zulu Folk Medicine.
Palabras clave: Medicina Tradicional; Plantas Medicinales Sudafricanas;
Epilepsia; Remedios Anticonvulsivantes Indgenas; Medicina Popular Zul.
Ojewole: Indigenous Remedies and Epilepsy
INTRODUCTION
The devastating cortical disorder named epilepsy
afflicts people of both sexes and of all age groups.
Current estimates suggest that more males than
females are susceptible to epileptic seizures, and
that about 6% of the worlds population suffer from
the central nervous system (CNS) disorder. The
term epilepsy, sometimes referred to as
convulsion, derives from the belief that in the olden
days, people whose bodies were possessed by evil
spirits always suffered from the disease. The name
epilepsy was actually derived from a Greek word
meaning to seize hold of. Nowadays, however, this
Holy Disease of the Greeks and of Medieval Ages
is regarded as a functional disorder of the brain,
and represents the clinical manifestation of a
paroxysmal electrochemical disturbance in the
central nervous system. Indeed, epilepsy is now
regarded as a chronic brain disorder characterized
by the tendency of the sufferer to experience
periodic, unpredictable recurring seizures that vary
in severity and appearance, and may or may not be
accompanied by convulsions. The term seizure
refers to a transient alteration in a patients
behaviour due to an abnormal, disordered,
synchronous, rhythmic firing and excessive
electrical discharge of populations of his/her brain
neurons. A seizure is referred to as nonepileptic
when it is evoked in a normal brain by a treatment
such as electroshock or a chemical convulsant.
However, a seizure is said to be epileptic when it
occurs without evident provocation. The term
seizure describes various experiences and
behaviours of the sufferer, and is not exactly the
same as convulsion, although the two terms are
often used synonymously. Convulsions are violent
fits in which abnormal movements of the body
occur owing to involuntary muscular jerking and
spasms, which may or may not be accompanied by
partial or total loss of consciousness. Anything that
irritates the brain can produce a seizure. A seizure
usually lasts for 2 - 5 minutes. When it stops, the
patient may have a headache, sore muscles,
unusual sensations, confusion, and profound
fatigue - called postictal state. Usually, the patient
does not remember what happened to him/her
during the seizure period. No consistent
biochemical defect has been demonstrated in
epileptic attacks. However, birth injury, brain
neoplasm, brain trauma and/or infection increase
the likelihood of epilepsy. In susceptible individuals,
attacks may be spontaneous, and/or can be
precipitated by flashing lights, exhaustion and
stress. These factors are used in the diagnosis of
epilepsy when attacks are induced under controlled
conditions.

Epilepsy may arise from an unknown cause (i. e.,
primary or idiopathic epilepsy). Alternatively, it may
develop secondary to, or as a consequence of,
some diseases or other known factors which affect
the brain. Such secondary factors include: brain
injury at birth or later in life, cerebral tumour or
trauma, genetic disorders, drug/alcohol withdrawal,
microbial infection, developmental abnormalities,
cerebrovascular disease, metabolic disturbances
and biochemical insults to the brain - such as
hypoglycaemia, anoxia, hypocalcaemia, illicit drug
use, and so on. Epilepsy of known origin or cause
is called secondary or symptomatic epilepsy.
Correct diagnosis of the type of epilepsy is
important as drugs may selectively benefit certain
classes of epileptic patients only. Uncontrolled
epilepsy is debilitating and can severely interfere
with the patients daily life activities and those of
his/her family.

The relationship between epilepsy and its
behavioural or mental associations has always
been a matter of great interest, debate and
controversy. However, it is always useful to
consider historical perspectives, and some of our
ancestors observations, views and opinions on
epilepsy before going into detailed account of the
disorder.

There is an enormous historical legacy which has,
no doubt, shaped our perception as well as the
publics attitudes to epilepsy. The Greeks of the
Graeco-Roman Period believed that epilepsy is a
sacred disease that is caused by the invasion of
the body by a god. This belief is based on the
assumption that only a god could deprive a healthy
man of his senses, throw him to the ground,
convulse him, and then rapidly restore him to his
former self again. The Greeks of the Medieval
Ages also believed that gods occupied heavenly
spheres, one of which was the moon. Hence, the
term lunatic was applied to sufferers of epilepsy.
On the other hand, mad people were regarded as
maniacs whose madness was due to invasion of
their bodies by devils or evil spirits. However, the
distinction soon became blurred and epileptic
patients were regarded as both lunatics and
maniacs. In the worlds first scientific monograph
on epilepsy (titled: On The Sacred Disease),
Hippocrates disputed the myth that the cause of
epilepsy is supernatural, that the human body
could be polluted by a god, and that the cure is
magic. He hypothesized that epilepsy is a disease
of the brain which could be treated by diet. At the
same time, Hippocrates distinguished primary, true
or idiopathic epilepsy (a disorder of an unknown
cause) from secondary, symptomatic or organic
epilepsy (a disorder resulting from a known
pathological state).
The process of distinguishing epilepsy from
madness began in the 19
th
century, and was linked
with the development of NEUROLOGY as a new
and autonomous medical science discipline (1). At
the beginning and throughout most of the 19
th

century, epilepsy was primarily the concern of the
alienists, the forerunners of modern psychiatrists,
who were then in charge of institutions such as the
Salptrire, in France (1). The French alienists
Morel and Esquirol, were influential in perpetuating
the view that most epileptic patients were mentally
disturbed. Indeed, Morels famous degeneracy
theory was applied to the mentally ill with or without
epilepsy (1). For many years, epilepsy remained an
integral part of psychiatric nosology. It was the new
breed of neurologists who began to challenge
these deeply entrenched concepts as they
encountered much epileptic patients without mental
impairment or illness in their private practices (1).
According to Berrios (1984) (2), as the neurological
perspective of epilepsy began to develop, the
psychiatrists invented a new strategy for keeping
epilepsy in the psychiatric camp. New and obscure
terms and forms of epilepsy, such as larval or
masked epilepsy, or even epileptic equivalent were
invented and hypothesized to embrace vaguely
paroxysmal forms of psychological disorder in the
absence of any overt seizure. The French
psychiatrists, Morel (1860) and Falret (1860), were
again in the forefront of this movement (1).
However, following the discovery in the 1930s, of
electroencephalography (EEG) by Berger, newer
terms and words such as subclinical and subictal
epilepsy were introduced to replace the earlier
inventions.

In the latter half of the 19
th
century, views about
epilepsy were drastically changed by Jackson
(1873)(3), who suggested that the word epilepsy
should be re-defined in neurophysiological rather
than clinical terms as follows:

Epilepsy is the name for occasional, sudden,
excessive, rapid and local discharges of the grey
matter.

This was the first neuronal theory of epilepsy, and
laid the foundation stone of our modern
understanding of the disease (1). This semantic
retreat by Jackson is apparently not well known
and understood. It was later overtaken by the
discovery of electroencephalography (EEG) by
Berger. Although Berger himself did not understand
English, and possibly had never had of Jackson,
and much less read his papers, a later generation
of clinical neurophysiologists were convinced that
the spikes and other epileptiform tracings that
Berger and his successors had discovered,
corresponded with Jacksons intuitive neuro-
physiological definition of epilepsy (4). One spin-off
from Jacksons neurophysiological definition of
epilepsy was that it thereafter became possible to
classify the mental manifestations of epilepsy into
ictal and interictal, and later, into peri-ictal or
postictal (1). Jacksons original descriptions of
dreamy states represented an early attempt at
defining ictal mental states (1).

At the beginning of the 20
th
century, the
psychiatrists views about epilepsy still dominated
the medical literature (1). Guerrant et al., (1962) (5)
described three new phases of evolutionary
thinking. In the early part of the 20
th
century, the
concept of the epileptic character held sway (1).
According to this view, the epileptic patient could
be identified by his vulnerability to certain
personality traits, mostly of an unfavourable or
antisocial nature. Later in the century, it became
more widely accepted that most epileptic patients
had normal mental states. This was really an
extension of the observations first hinted at by the
19
th
century neurologists. The culmination of this
process is that only within the last 45 years has the
diagnosis of epilepsy per se been finally removed
from the international classification of psychiatric
illnesses (1). The publication of Gibbs et al., (1948)
(6) ushered in what Guerrant et al. (1962) (5) have
described as the era of psychomotor peculiarity. In
their electrophysiological study of patients with
psychomotor seizures, Gibbs et al., (1948) (6) were
impressed with the association of EEG
abnormalities in the anterior temporal area and
disturbances in personality. Since then, the
concept has expanded. An enormous and
controversial literature has since evolved, relating
temporal lobe epilepsy not only to personality
disorder, but also to aggression, schizophrenia-like
psychoses, and so forth (1). The latter part of the
20
th
century was characterized by steadily
increasing scientific study of the relationships
between epilepsy and mental disturbance of all
kinds (1). Epidemiological studies (7) have
suggested that as many as one-third or more
epileptic patients with active epilepsy have
significantly disabling additional psychological
problems that range in character from cognitive
impairment and behavioural disorders to
depression and anxiety. Instead of all-embracing
degeneracy, personality and temporal lobe
theories, recent research endeavours have begun
to concentrate on the wide range of complex
biological and psycho-social factors which exert
their influences to varying degrees in children,
adolescents and adults with epilepsy (1). These
include the effects of: seizures of different types
and combination, the duration and severity of the
epilepsy, the age of onset of the disorder and the
degree of maturation of the nervous system, the
site and degree of brain damage, whether pre- or
postictal, the amount and duration of antiepileptic
therapy and its metabolic consequences, genetic
factors, electroencephalographic abnornalities,
neurophysiological mechanisms, and the influence
of family, school, employment (or lack of it), and a
whole range of environmental, social and
psychodynamic psychometric performance,
behaviour and psychopathology, and so on (1).

Epilepsy appears in a variety of forms. All types of
epilepsy involve recurrent disturbances of the brain
activity, which may be symptomless (but detectable
by EEG) or involve motor, sensory and/or psychic
disturbances. It may present as a generalized
disturbance of cerebral function (i.e., general
epilepsy), or as a localized disturbance of such
cerebral function (i.e., focal epilepsy). Hereditary
factors play a role in some, but not in all, cases of
idiopathic epilepsy. In general epilepsy, and some
forms of focal epilepsy, patients are subjected to
attacks in which consciousness is partially or
completely lost. The severe forms of general
epilepsy are known as major epilepsy (i. e., grand
mal epilepsy) and in these forms of epilepsy, loss
of consciousness is usually accompanied by
muscular contractions, producing what are usually
termed epileptic fits or epileptic seizures. Such fits
do not occur in the milder forms of the disease
which are termed minor epilepsy or petit mal
epilepsy. Radiological investigations and
electroencephalography (EEG) are valuable aids in
differentiating between idiopathic and symptomatic
epilepsy. Classically, in a grand mal epileptic
attack, an initial transient aura is followed by a tonic
convulsion, in which all muscles contract and
consciousness is temporarily lost. The patient falls
to the ground, and after 15 60 seconds exhibits a
clonic convulsion, where major groups of muscles
contract and relax alternately. Clonic movements of
the jaw and lips cause the saliva to froth (frothing at
the mouth), and usually, there is urinary and faecal
incontinence. The convulsion ceases after about
1 2 minutes, but the patient may remain
unconscious for up to 1 hour. On recovery, there is
usually confusion and total amnesia about the
episode. All these stages are not always present in
every epileptic attack. Petit mal epilepsy is
characterized by the brevity of the attacks. They
may simply involve a clouding of consciousness for
a few seconds, which are then termed absences.
There are no convulsions, but up to 100 such
absences may occur each day. Other types of
epilepsy, such as focal epilepsy or psychomotor
epilepsy also exist, where the disturbance is
confined to a particular area of the cortex or to the
temporal region, respectively. Mixed types are
common. Epileptic attacks are associated with a
spreading abnormal electrical discharge, initiated at
a focus in the brain. The type of epilepsy and
extent of symptoms depend on which particular
areas of the cortex are involved.

In children, convulsion is known to cause mental
retardation, and an uncontrolled fit can lead to
paralysis of limbs, unconsciousness, and even
death (8, 9). In the early nineteenth century, two
proposals were put forward as to the causes of
epilepsy. The first was that epilepsy is a single
disease entity, and that all forms of it have a
common cause. On the other hand, the second
opinion proposed that different types of epilepsy
result from different chemical, anatomical, or
functional (physiological) disorders. However, the
consensus of opinion at the Symposium on
Evaluation of Drug Therapy in Neurological and
Sensory Diseases was that: Epilepsy is a symptom
complex characterized by recurrent paroxysmal
aberrations of brain functions, usually brief and
self-limited (10).

It is now generally believed that all forms of
epilepsy originate in the brain as a result of
changes in neuronal electrochemical activity.
These changes, such as excessive neuronal
discharge, may in turn, be brought about by a
disturbance of physico-chemical function and/or
electrical activity of the brain. The cause of this
abnormality is, however, not fully understood (11).
Attempts to classify epileptic seizures have only
been partially successful, mainly because of the
limited knowledge of the pathological processes of
the brain involved in the disorder. In 1981, the
Commission on Classification and Terminology of
the International League Against Epilepsy put
forward a new proposal, a short version of which is
based on clinical seizure type, ictal (seizure-
induced) electroencephalographic (EEG)
expression, and interictal (occurring between
attacks or paroxysms) EEG expression (11).

To date, there is no single unifying explanation as
to how the diverse secondary factors (mentioned
earlier) cause seizures. Mechanisms that
precipitate epilepsy remain difficult to clarify and
explain. However, it has been possible to
investigate the physiological events that actively
participate in the pathogenesis of epilepsy. The
pivotal role of synapses in mediating
communication among neurons in the mammalian
brain suggested that defective synaptic function
might lead to a seizure. That is, a reduction of
inhibitory synaptic activity, or an enhancement of
excitatory synaptic activity, might be expected to
trigger a seizure. The widely accepted cellular
hypothesis indicates that two primary factors
produce seizures. These are: (i) increased
excitability of the brain neurons, and (ii)
synchronization of neuronal populations in the
brain (12, 13). Under normal physiological
conditions, the membrane potential of the brain
neurons is determined by ionic concentration
gradients. Ionic changes in the environment of the
epileptic foci can contribute to the instability of the
neurons. The neurotransmitters mediating the bulk
of synaptic transmission in mammalian brain are
amino acids. Examples of such amino acids
include excitatory amino acids (EAAs) like
glutamate and aspartate, and inhibitory amino
acids (IAAs) such as gamma-aminobutyric acid
(GABA) and glycine. These EAAs and IAAs are the
most abundant neurotransmitters in the CNS, and
are used for neurotransmission in most clinically
relevant pathways of the brain. Both the EAAs and
IAAs have been reported to play crucial roles in the
pathogenesis of epileptic seizures (13, 14).

Glutamate is the most important excitatory
neurotransmitter in all rapidly conducting relay
pathways of the motor and sensory systems of the
outer tube of the CNS. It produces fast and
prolonged synaptic excitation, and triggers various
calcium-dependent processes in the target cells,
including production of nitric oxide. Glutamate also
plays a major role in synaptic plasticity during
development, and in the processes of learning and
memory (13). During an epileptic attack, the brain
neuronal membrane potential suddenly drops and
remains depolarized, at least for some seconds,
before returning to normal. This event results from
the abnormally exaggerated and prolonged action
of an excitatory neurotransmitter. Activation of
glutamate N-methyl-D-aspartate (NMDA) receptors
is believed to play a major role in this event.
Activation of glutamate NMDA receptors produces
a voltage-dependent blockade of magnesium ions,
subsequently leading to depolarization. There is an
overwhelming evidence in the medical literature
indicating that enhancement of glutaminergic
neurotransmission is responsible for the discharge
and/or firing of the brain neurons resulting in
epileptic attacks; whereas its reduction results in
the antagonism of seizures (12, 14). The search for
selective glutamate antagonists has helped in the
better understanding of the physiological role of the
different types of excitatory amino acid receptors,
and in the development of potential therapeutic
agents for the treatment and/or management of
some neuro-degenerative diseases and epilepsy.
Glutamic acid receptor agonists mimic the action of
glutamic acid at the glutamate NMDA receptors,
and induce epileptic seizures. A good example of
such convulsant agents is N-methyl-D-L-aspartic
acid (14).

Gamma amino butyric acid (GABA) is the main
inhibitory neurotransmitter in the CNS, and is
particularly abundant in the brain. There are three
main subtypes of GABA receptors, namely:
GABA
A
-receptors which are members of the ligand-
gated, ion-channel superfamily, GABA
B
-receptors
which are members of the G-protein linked receptor
superfamily, and GABA
C
-receptors which have just
been lately discovered. All these GABA receptors
have been cloned, and have shown many features
in common with glutamate receptors. GABA
A
-
receptors are post-synaptically located, and they
mediate fast postsynaptic inhibition of neuronal
excitability. GABA
B
-receptors, on the other hand,
are located pre- and post-synaptically on the
neurons. They closely resemble metabotropic
glutamate receptors. They act by binding to
voltage-gated calcium channels, resulting in
reduced neurotransmitter release from neuronal
terminals, and also by opening potassium
channels, thereby producing reduced postsynaptic
excitability (14). GABA
C
-receptors are selectively
activated by the non-selective agonists of GABA
and show no preference for benzodiazepines,
barbiturates, or neuro-steroids. Like GABA
A
-
receptors, GABA
C
-receptors are linked to chloride
ion channels that are normally inhibited by
picrotoxin. GABA is thought to function as an
inhibitory neurotransmitter in different CNS
neuronal pathways. The widespread distribution of
GABA in the brain, coupled with the fact that
virtually all CNS neurons are sensitive to its
inhibitory effect, suggest that the inhibitory function
of GABA is ubiquitous in the brain. Stimulation of
GABA
A
-receptors reduces the depolarization
produced by excitatory neurotransmitters, and thus
stabilise membrane potentials so that the
membrane is unable to respond to excitatory
stimuli. Thus, GABA
A
-receptor stimulation helps to
contain neuronal discharges, and consequently,
drugs which block GABA
A
-receptors will, therefore,
produce seizures. In general, enhancement of
GABAergic neurotransmission may antagonize
epileptic attacks, whereas its inhibition may result
in epileptic attacks (12, 13, 14). GABA
A
-receptors
are targets for certain centrally-acting drugs,
especially benzodiazepines, barbiturates, and
neurosteroids. A classical example of GABA
A
-
receptor agonist is muscimol, a drug which
hyperpolarises GABA-sensitive neurons.
Bicuculline, a naturally-occurring convulsant drug,
is a specific antagonist of GABA
A
-receptors.
Bicuculline acts by selectively blocking the action of
GABA on GABA
A
-receptors, which control chloride
ion permeability. Pentylenetetrazol (i. e.,
metrazol), another convulsant agent, acts by
antagonising the action of GABA at GABA
A
-
receptors. Picrotoxin is also a convulsant drug
which acts by blocking the chloride ion channels
associated with GABA
A
-receptors, thus blocking
the postsynaptic inhibitory effect of GABA.
Although these compounds are useful in
experimental studies, they have no therapeutic
value.

Benzodiazepines (BDZs) selectively potentiate the
effects of GABA on GABA
A
-receptors, and thus
produce broad anticonvulsant properties. They bind
with a high affinity to an accessory site (known as
benzodiazepine receptors) on GABA
A
-receptors.
The binding of GABA to GABA
A
-receptors is then
facilitated, and its agonistic action exacted through
GABA-mediated opening of the chloride ion
channels, is enhanced. Diazepam has a well-
defined role in the management of status
epilepticus for which it is the first-line drug and
indeed, the drug of choice. However, its relatively
short duration of action constitutes a major
drawback. Other modulators which enhance the
action of GABA include CNS depressants such as
barbiturates and neurosteroids. Barbiturates act by
enhancing the inhibitory effect of GABA on GABA
A
-
receptors, and facilitating GABA-mediated opening
of chloride ion channels. An example of
barbiturates that is commonly used in the
management of epilepsy is phenobarbitone. This is
an effective drug for generalized tonic-clonic, and
partial seizures (14). Other clinically effective
antiepileptic drugs, such as phenytoin and
carbamazepine, affect cortical neuronal membrane
excitability by an action on voltage-dependent
sodium channels, which carry the inward current
necessary for the generation of an action potential.
They preferentially block the excitation of brain
neuronal cells that fire repetitively at high
frequencies (14). Pharmacologically, the intended
effect of anticonvulsant drugs is to attenuate or
suppress seizure discharges. It is paramount to
note that excessive GABA inhibition may limit
normal CNS functions, and anticonvulsant drugs
have the potential for causing sedation when used
in excessive amounts.

The various types of chemical substances used in
the prevention, management and/or control of
epilepsy are collectively known as anticonvulsants.
Idiopathic epilepsy is treated by daily administration
of anticonvulsant drugs, with the aim of preventing
the attacks, or reducing their severity and
frequency. It should be noted, however, that drug
therapy does not cure, but merely controls, the
symptoms of epilepsy. Nevertheless, cures do
occur, but they are more likely to be spontaneous,
rather than drug-induced. From the Middle Ages to
date, drugs used in the control epileptic seizures
have been mainly synthetic. They include such
simple chemical compounds as inorganic salts like
potassium bromide and magnesium sulphate;
alcohols like isopropyl alcohol; barbiturate
derivatives; carbamate derivatives; propanediols;
hydantoins; glutarimides; succinimides;
oxazolidinediones; and so on. Treatment of
epilepsy or convulsion in the Middle Ages
emphasized substances of occult power, frog's
liver, and human urine, preferably collected from
the first witness to the seizure. In 1975, the
Epilepsy Branch of the National Institute of
Neurological and Communicative Disorders and
Stroke (NINCDS) established an anticonvulsant
drug screening project that is still on going. Since
1975 to date, however, thousands of chemical
compounds have been tested for anticonvulsant
and neurotoxicity activities. The strategy of testing
involves determination of the anticonvulsant activity
by a catalogue of tests. These tests detect, on one
hand, the anticonvulsant activity resulting from the
prevention of seizure spread and, on the other
hand, the anticonvulsant activity related to the
elevation of seizure threshold. The sequence of
testing consists of determination of the
anticonvulsant activity in laboratory animals in
electrically- and chemically-induced seizures,
followed by determination of the acute toxicity.
According to Toman (1965) (15), the ideal
antiepileptic drug, among other things, should
completely suppress seizures in doses that do not
cause sedation or other undesirable CNS toxicity. It
should be well tolerated and highly effective
against various types of seizures, and devoid of
adverse effects on vital organs. Its onset of action
should be rapid after parenteral administration for
the control of status epilepticus, and it should have
a long duration of action after oral administration
for prevention of recurrent seizures.

The cellular mechanism of action of anticonvulsant
drugs is complex and not fully understood.
However, the commonly-used antiepileptic drugs
are thought to act mainly by two general
mechanisms in which they may abolish or
attenuate seizures. Anticonvulsant agents may act
by reducing electrical excitability of brain neuronal
cell membranes, possibly by blocking sodium ion
channels; or by enhancing GABA-mediated
synaptic inhibition. This may be achieved by an
enhanced postsynaptic action of GABA, by
inhibiting GABA-transaminase, or by direct GABA
agonistic properties. Additionally, some drugs
appear to act by a third mechanism which involves
inhibition of T-type calcium channels. A number of
newer antiepileptic drugs act by blocking excitatory
amino acid receptors. Most of these drugs are only
effective in experimental animal models and not in
clinical situations, probably because of their poor
ability to penetrate, or total inability to cross, the
blood-brain barrier. However, new anticonvulsant
agents available for clinical use include lamotrigine,
which is thought to act by inhibiting the release of
the excitatory neurotransmitter glutamate; and
topiramate which has been suggested to act by
multiple mechanisms, including glutamate receptor
antagonism (16, 17). At the cellular level, many of
the currently-available anticonvulsant drugs
enhance GABA-mediated synaptic inhibition in
cortical structures. Vigabatrine, a recently
introduced anti-epileptic drug, is thought to act by
inhibiting the enzyme GABA-transaminase, which
is responsible for inactivating GABA. Tiagabine
inhibits GABA uptake. All these activities lead to an
enhancement of GABA action as an inhibitory
neurotransmitter (14, 18).

The first effective antiepileptic remedy, potassium
bromide, was introduced by Locock in 1857 (19).
This agent was largely replaced by phenobarbitone
in 1912 when Hauptmann (1912) (20) tried this
sedative drug in epilepsy. Its great value was
recognised immediately, and to date,
phenobarbitone is still one of the best
anticonvulsant drugs available. Although the
usefulness of both bromide and phenobarbitone in
convulsive disorders was discovered by chance,
phenytoin was developed in 1937 as the result of a
study of potential anticonvulsant drugs in animals.
Phenytoin turned out to be highly effective in man,
and is non-sedative. Although management of
convulsive disorders by bromide, phenobarbitone
and phenytoin constitutes an important
advancement in the pharmacotherapy of epilepsy,
many other drugs have been introduced since
1937, with the hope that they might be non-toxic,
non-sedative anticonvulsants. To date, however,
many potential compounds of plant, animal and
mineral origins are continually being tested for
anticonvulsant properties.

The use of indigenous anticonvulsant remedies in
the control of epilepsy is as old as when epilepsy
itself was first recognized. Although the herbal
doctor may not comprehend the detailed chemical,
biochemical, pharmacological and nutritive values
of his/her medications, years of committed
observation, long-term practice and experience
with herbal drugs usually prove valuable in the
healers ability to manage epilepsy successfully
and effectively.

Among the Zulu people living in rural communities
of South Africa, management and/or control of
epilepsy is/are often achieved through the use of
herbal preparations. Some of the anticonvulsant
remedies are formulated in soap form, and patients
suffering from the malady are made to wash and/or
bath with the soap. In some communities, epilepsy
is considered to be an affliction caused by
supernatural powers, such as witches, wizards
and/or ancestral spirits. In such cases, the
convulsive disorders are usually not controlled with
herbal remedies alone, but also with exorcisms,
and/or incantations. Curing rites or sacrifices are
made to invoke the goodwill of the ancestors, and
appeal to the witches and wizards for forgiveness
of sins. The sacrifices are usually directed to the
body and mind of the convulsing patient. The body
of the patient is usually massaged with the
anticonvulsant remedies. More often, concoctions,
infusions, decoctions, tinctures or powders of the
anticonvulsant preparations are administered
orally. Baths in the herbal concoctions are
sometimes prescribed.

In the last three decades, traditional systems of
medicine have become a topic of global interest
and importance. Current estimates suggest that, in
many developing countries of the world, a large
proportion of the people still rely heavily on
traditional healers and medicinal plants for their
daily primary health-care needs. Although modern
medicine may be available in these countries,
herbal medicines (phytomedicines) have often
maintained popularity among the people for
historical, cultural and economic reasons. In South
Africa, plants have been used traditionally for
medicinal purposes for many centuries. With over
30 000 species of higher plants, medicinal plants
constitute the floristic wealth and an important
socio-cultural heritage of South Africa. The rich
cultural and bio-diversity of South Africa have
made it possible to use approximately 3 000 plant
species as medicines, out of which about 350
species are the most commonly-used and traded
medicinal plants (21). Some of the plants have also
been used for magical, ritual, spiritual and symbolic
purposes in addition to their medicinal and nutritive
values. The remarkable cultural diversity of South
Africa is reflected in the formal and informal
systems of medicine that are currently being
practised in different parts of the country. The
informal, oral-tradition medical systems of many
tribes in the country have not yet been
systematised, and are only passed on by words of
mouth from one generation to the other. These
medical systems and their herbal, animal and
mineral materia medica have ancient origins which
may date back to Palaeolithic times (21). The
formal systems of medicine, which are well
documented and systematised, were introduced to
the country over three centuries ago by European
and other settlers, and are exemplified by todays
modern, Western medicine. Ayurvedic medicine
from India, Traditional Chinese Medicine and
homoeopathic medicine are also being commonly
practised in South Africa (21). Each system of
medicine is the art and science of diagnosing the
cause/s of a disease, treating disease/s, and
maintaining good health in the broadest sense of
physical, spiritual, social and psychological well-
being. Each culture has found solutions to the
preventive, promotive and curative aspects of
health that resonate in harmony with the worlds
view of that culture (21). First and foremost, an
African traditional healer always seeks to know why
a patient is ill. Thereafter, s/he administers
treatment/s that will address the perceived cause/s
of the illness, in addition to other specific therapies
that s/he may administer to alleviate the signs and
symptoms of the disease.

There are an estimated 200 000 indigenous
traditional healers in South Africa, and about 80%
of South Africans still consult these healers, usually
in addition to using modern, Western medical
services (21). Traditional healers in South Africa
are most commonly known and referred to as
izinyanga and izangoma (Zulu), ixwele and
amaquira (Xhosa), nqaka (Sotho), bossiedokter
and kruiedokter (Western and Northern Cape). The
Zulu terms inyanga and isangoma used to refer
exclusively to herbalist and diviner respectively, but
in modern times, the distinction has become
blurred, with some healers practicing both arts (21).

In addition to the herbalists and diviners who are
believed to be spiritually endowed and empowered,
there are also traditional birth attendants, prophets,
spiritual healers, intuitives and dreamers in South
Africa. Most elderly folks in rural areas of the
country have knowledge of herbal lore, and
function as first-aid healers with a family repertoire
of herbal remedies or kruierate (21). Medicinal
plants constitute the link-pin of the various
traditional healers. These practitioners usually
employ galenicals (in the forms of infusions,
decoctions, concoctions, tinctures, powders, soaps,
etc), made from various morphological parts of
plants, especially twigs, leaves, stem- and/or root-
barks, wood, fruits, seeds, gums, nectar and so
forth, to treat their epileptic patients.

Although medicinal plants have been used for
millennia in the effective treatment and/or
management of various human and veterinary
ailments in South Africa, only a few of the South
African indigenous medicinal plants have been
examined scientifically for their medicinal values.
The core aims of this study were to review, collate
and screen pharmacologically, using mammalian
experimental animal models, some of the South
African indigenous medicinal plants that are
frequently used as antiepileptic remedies in Zulu
folk medicine. The Zulu Tribe of South Africa
constitutes one of the most culturally advanced,
socially distinct and very popular tribes in South
Africa. From ancient times, the Zulu people of
South Africa have employed indigenous remedies
to treat and/or manage a plethora of human
ailments, including epilepsy and convulsions.

MATERIALS AND METHODS

PLANT MATERIAL

A literature search (21, 22, 23, 24) on the medicinal
plants examined in this study was undertaken to
know their chemical constituents and accredited
medicinal uses. Collection of the various
indigenous antiepileptic plants and recipes, visits to
traditional healers in KwaZulu-Natal, and
pharmacological screening of the plant extracts for
antiepileptic activities started in August 1998, and
ended in July, 2001. The various plant materials
tested were identified by the Taxonomist/Curator of
the University of Durban-Westvilles Department of
Botany, Durban, South Africa; and/or by the staff of
the Natal Provincial Herbarium in Durban, South
Africa (where voucher specimens of the plants
have been deposited). One kilogramme (1 kg) each
of the most commonly-employed morphological
parts of the medicinal plants (as used traditionally
in Zulu folk medicine for the treatment of
epilepsy/convulsion), were separately washed with
clean tap water, dried, cut into smaller pieces and
homogenized in a Waring blender. Each
homogenate was Soxhlet extracted twice, on each
occasion with 2.5 litres of distilled water at a
temperature of 30 1
o
C for 24 hours with shaking.
The combined extracts were filtered and
concentrated to dryness under reduced pressure at
30 1
o
C. The resulting plant extract in each case
was freeze-dried, finally yielding powdery or semi-
powdery, crude aqueous extract residues. Aliquot
portions of the aqueous extract residue from each
of the plants examined were weighed out and
dissolved in distilled water for anticonvulsant
evaluation on each day of our experiment.
ANIMAL MATERIAL

For each of the plant extracts examined, mice of
both sexes (Mus domesticus) weighing 25 30 g
were used. The mice were randomly divided into
three groups of Test A, Test B and Control C
mice. Eight (8) mice were used for each test
compound, and an equal number of mice were also
used as controls in each case. Convulsive
seizures were chemically-induced in the test
animals as described in detail earlier by Ojewole
(2000) (25) Pentylenetetrazol [i. e., metrazol (PTZ
90 mg/kg ip)] and picrotoxin (PIC, 10 mg/kg ip.)
were used to induce chemoshock seizures in the
mice. Each of the control animals in Control C
group was treated with distilled water (2 ml/kg ip)
only. Phenobarbitone (10 mg/kg ip) and diazepam
(0.5 mg/kg ip) were used as standard, reference
anticonvulsant drugs for comparison with the plant
extracts.

DATA ANALYSIS

Experimental data obtained from test mice treated
with the plant extracts and standard anticonvulsant
drugs used, as well as those obtained from distilled
water-treated control mice, were pooled and
expressed as percentages arising from differences
between treated and non-treated groups, and are
referred to the control treated only with the
convulsant agent. Differences between the plant
extract- and reference anticonvulsant drug-treated
test means, and distilled water-treated control
means, were analyzed statistically. Students t-test
[26] was used to determine the level of significance
of the difference between the test and control
group data means. Values of p 0.05 were taken
to imply statistical significance.

RESULTS
Our ethnobotanical literature survey revealed that
a large number of medicinal plants from various
genera and diverse families (especially,
Asteraceae, Bignoniaceae, Fabaceae,
Verbenaceae, Rubiaceae, Rutaceae,
Commelinaceae, Meliaceae, Lamiaceae,
Solanaceae, Apocynaceae, Euphorbiaceae,
Myrtaceae, Polygonaceae, Rosaceae,
Crassulaceae, Sapotaceae, Capparaceae,
Vitaceae, and so forth) are used in Zulu folk
medicine for the control or management of
epilepsy/convulsions.
Thirty-five of the medicinal plants frequently used
as antiepileptic remedies in Zulu folk medicine
were collated, reviewed, collected, and
authenticated. Aqueous extracts of their most
frequently-used morphological parts were
pharmacologically screened for anticonvulsant
activities in experimental, mammalian animal
model. The local (Zulu) names of the plants, their
morphological parts commonly used by Zulu
traditional healers as antiepileptic and/or
anticonvulsant remedies, their chemical
constituents and accredited medicinal uses, as well
as their relative anticonvulsant properties in
chemically-induced seizures, are summarized in
Table 1.

Pharmacological evaluation of the various plant
extracts (and the reference antiepileptic drugs used
in this study) showed that moderate to high doses
of the plant extracts ( 800 mg/kg ip) produced
moderate to strong anticonvulsant activities in the
mammalian experimental animal model used. On
their own, phenobarbitone (10 mg/kg ip) and
diazepam (0.5 mg/kg ip) produced very strong,
pronounced and significant (P < 0.01 0.001)
anticonvulsant effects in the mice, offering 100%
protections against metrazol- and picrotoxin-
induced seizures respectively (figures not shown).
The percentage anticonvulsant actions of the
various plant extracts were calculated relative to
those produced by phenobarbitone and diazepam.
The magnitude of the anticonvulsant effects of the
plant extracts varied widely. Except in 2 cases, the
plant extracts were generally more effective in
protecting the animals against metrazol-induced
seizures than in protecting the mice against
picrotoxin-induced seizures. Of the 35 different
plant extracts examined, 17 (ie, 48.57%) produced
significant (P < 0.05 0.001) moderate to strong
anticonvulsant effects in metrazol-induced,
chemoshock seizures (producing 62.50% 87.50%
protections against metrazol-induced seizures in
the mice). The remaining 18 of the 35 (ie, 51.43%)
plant extracts showed weak to mild anticonvulsant
activities (producing 12.50% 50.00% protections
against metrazol-induced seizures in the animals).
Maximal anticonvulsant effects of the plant extracts
were elicited at doses 800 mg/kg ip, 15 30
minutes post administration.


Table 1. Some South African medicinal plants used as anticonvulsant remedies in Zulu folk medicine.

#

Family
Species
[Zulu name]

Parts
Used

Chemical Constituents

Medicinal Uses
%
protection
against
metrazol -
induced
seizures
%
protection
against
picrotoxin-
induced
seizures
1. Anacardiaceae
Lannea discolor
(Sond) Engl.
[isiganganyane]
Leaves
Stem-bark
Roots
Flavonoids,
polyphenolics and
tannins.
Convulsions and fits, diarrhoea,
abscesses and boils, infertility,
menorrhagia, sore eyes gonorrhea,
swollen legs and whooping cough.

25.00

25.00
2. Apocynaceae
Rauvolfia caffra
Sond.
[umhlambamazi]
Stem-bark
Root-bark
Leaves
Indole and indoline
alkaloids, rauvolfine,
reserpine, yohimbine,
ajmalicine and
phytosterols.

Hypertension, malaria, fevers, colic
pains, rheumatism, pneumonia, mental
problems, insomnia and hysteria,
rashes, convulsions, asthma, cough
and other chest complaints.

87.50

75.00
3. Asteraceae
Blumea alata (D.
Don) DC.
[ugodide]
Roots
Leaves
-Humulene,
caryophyllene and
squalene, minute
amounts of cuathemone
derivatives.
Fevers, convulsions, constipation,
colic and abdominal pains,
pneumonia, heart pains, headaches
and leg pains, and Trichomonas
vaginalis infection.

37.50

12.50

4. Asteraceae
Conyza scabrida
DC.
[uhlabo]
Leaves
Roots

Diterpenoids, hautriwaic
acid, and clerodane
derivatives.
Convulsions, colds and coughs,
pleuritic pains, headaches, fevers,
chest and heart complaints.

75.00

62.50
5. Asteraceae
Vernonia
neocorymbosa
Hilliard
[uhlungu-lungu]
Leaves
Twigs
Roots

Squalene, vernolide and
vernodalin,
sesquiterpenoid
lactones, flavonoids,
pyridine, and diterpenoid
alkaloids.
Epilepsy, abortion, stomach ache,
hysteria , irregular menstruation,
dysentery and intestinal worm
infestations.

87.50

75.00
6. Bignoniaceae
Kigelia africana
(Lam.) Benth.
[umfongothi]

Fruits
Stem-bark
Flavonoids,
dihydroisocoumarin
kigelin, naphthoquinone
derivate lapachol, iridoid
glycosides, cinnamic
acid derivatives,
stigmasterols and -
sitosterol.
Ulcers, sores, syphilis, stomach
ailments, dysentery, constipation,
snakebite, wounds, boils and sores,
gynaecological disorders,
rheumatism, acne, pneumonia,
convulsions, aphrodisia,
haemorrhoids and lumbago.

75.00

50.00
7. Bignoniaceae
Tecomaria capensis
(Thunb.) Spach
[lungana]
Stem-bark
Leaves
Sterols and sterolins,
tannins and terpenoids.
Fevers, pains, insomnia, chest
complaints, diarrhoea, dysentery,
bacterial infections, stomach pains,
influenza, pneumonia and convulsions.

62.50

37.50
8. Capparaceae
Boscia albitrunca
(Burch.) Gilg & Ben
[umvithi]
Roots
Leaves
Fruits
Phytosterols and
sterolins.

Haemorrhoids, inflamed eyes,
epilepsy.

50.00

50.00
9. Capparaceae
Capparis tomentosa
Lam.
[umabusane]
Roots
Leaves

Oxindole compounds,
alkaloid stachydrine, and
sulphur oil.
Rheumatism, insanity, snakebite,
jaundice, chest pains, malaria,
headaches, pneumonia, coughs,
asthma, constipation, eye problems
and convulsions.

62.50

37.50
10. Celastraceae
Maytenus
senegalensis (Lam.)
Excell
[isihlangu]
Roots
Leaves
Polyphenolics, tannins
and terpenoids.
Haemoptysis, respiratory ailments,
epilepsy, body pains, constipation,
diarrhoea, night blindness, infertility,
menorrhagia, mouth ulcers and
wounds, sore throats, dysentery,
microbial infections and
schistosomiasis.

50.00

25.00

Table 1 (Continues)

11. Commelinaceae
Commelina africana
Linn.
[idangabane]
Roots Flavonoids, glycosides
and anthocyanin
derivatives.
Insomnia, infertility, epileptic fits,
heart complaints, nervous ailments,
venereal diseases, body pains,
menstrual and bladder
ailmemts.

75.00

50.00

12. Crassulaceae
Cotyledon orbiculata
Linn.
[intelezi]
Leaves
Leaf juice
Tyledoside and
bufadienolide-type
cardiac glycosides such
as orbicuside A, B, and
C.
Corns and warts, toothache and
earache, boils, inflammation,
rheumatism, epilepsy,
and syphilis.

62.50

75.00
13. Crassulaceae
Crassula alba
Forssk.
[isidwe]
Leaves
Twigs
Polyphenolics and
tannins.
Epilepsy, dysentery and diarrhoea,
bloody stools, influenza, fevers,
heartburn and hysteria.

50.00

50.00
14. Cucurbitaceae
Cucumis hirsutus
Sond.
[intangazane]
Roots
Fruits
Cucurmin, steroids and
saponins.
Coughs, constipation, abdominal
pains, convulsions, abortion, penal
and vulval sores.

25.00

12.50
15. Ebenaceae
Euclea divinorum
Hiern
[umhlangula]
Fruits
Roots
Stem-bark
Naphthoquinones,
diospyrin, lupeol and
betulin, triterpenoids,
saponins, tannins and
steroids.
Convulsions, toothaches,
constipation, schistosomiasis, chest
pains, pneumonia, gastric disorders,
infertility, swellings and inflammatory
conditions, headaches and depressed
fontanelles .

50.00

37.50
16. Euphorbiaceae
Croton gratissimus
Burch.
[umahlabekufeni]
Stem-bark/
Roots/
Leaves
Alkaloids, flavonoids,
saponins, cardenolides,
monoterpenoids and
diterpenoids, aromatic
oils, crotonin, crotin and
nuciferine.
Fevers, bleeding gums, rheumatism,
chest complaints, constipation and
indigestion, oedema (dropsy), coughs,
inflammation, insomnia, aphrodisia
and epilepsy.

25.00

12.50
17. Euphorbiaceae
Jatropha curcas
Linn.
[inhlakuva]
Roots
Seeds
Leaves

Oil containing tiglian-
type irritant diterpenoids,
curcanoleic acid, toxic
protein named curcin,
cyanic acid, flavonoids,
steroids, triterpenes and
oleic acid.
Constipation, boils and wounds,
dropsy, sciatica, paralysis, skin
diseases, sores, venereal diseases,
angina, herpes, malaria, jaundice,
fevers, diarrhoea, ringworm,
rheumatism, convulsions and fits.

50.00

50.00
18. Fabaceae
Abrus precatorius
Linn.
[umkhokha]
Roots
Leaves
Flavone, choline,
trigonelline, precatorine,
glycyrrhizin, abrin,
abrusogenin,
abrusosides, indole
derivatives and abrine,
saponins,
anthocyaninsns and the
steroids abricin and
abridin.
Love and good luck charms, pleuritic
chest complaints, eye ailments,
contraception, convulsions,
schistosomiasis, tuberculosis, warts
and skin diseases, snakebite,
intestinal worm infestations,
aphrodisia, bronchitis, asthma and
whooping cough, colds, fevers, and
malaria.

37.50

12.50

19. Fabaceae
Acacia karroo
Hayne
[umunga]
Stem-bark
Leaves
Gum
Polyphenols and
tannins, uronic acid,
galactan derivatives,
and sulphated
glycosides.
Diarrhoea and dysentey, conjunctivitis,
haemorrhage, colds, oral thrush,
stomach ache, osteomyelitis,
dizziness, convulsions, venereal
diseases and aphrodisia.

25.00

12.50

20. Fabaceae
Mimosa pudica Linn
[imbune]
Whole
plant
Mimosine and
norepinephrine.
Convulsions/epilepsy, dysmenorrhoea,
heart palpitations, insomnia and
nervousness.

12.50

12.50

Table 1 (Continues)

21. Lamiaceae
Leonotis leonurus
(Linn.) R. Br.
[umunyane]
Leaves
Stems
Roots
Volatile oil, diterpenoids,
labadane-type lactones,
premarrubiin and
marrubiin.
Epilepsy, snakebite and insect stings,
boils, eczema, skin diseases, itching,
muscular cramps, influenza, coughs,
colds, bronchitis and asthma,
hypertension, partial paralysis,
headaches and viral hepatitis.

87.50

37.50
22. Loganiaceae
Nuxia floribunda
Benth.
[ingobese]
Leaves/
Stem-bark

Polyphenolics and
tannins.
Fevers, coughs, indigestion, influenza,
and infantile convulsions.

37.50

12.50

23. Meliaceae
Melia azedarach
Linn.
[umsilinga]
Leaves
Root-bark
Heartwood
Oxidised triterpenoids
known as limonoids,
triterpenoid saponins,
steroids, aromatic
compounds, vanillic
acid, azedainic acid,
melianoninol,
coumarins, lignans and
flavonoids.
Abdominal pains, helmintiasis,
epilepsy, fits/convulsions,
schistosomiasis, swollen legs,
asthma, constipation, spasms and
nervous pains, eczema, malaria,
diuresis, rheumatism, gout and skin
diseases.

87.50

62.50
24. Phytolaccaceae
Phytolacca
dodecandra LHerit.
[umahedeni]
Roots
Leaves
Berries
Steroidal triterpenoid
saponins, endod
saponoside, lematoxin
and oleanonic acid
derivatives.
Urinary complaints, snakebite,
epilepsy, uterine tumors and fibroids,
rheumatism, inflammatory conditions,
fish poison, boils and wounds,
spermicidal contraception, syphilis and
other parasitic infections.

75.00

62.50
25. Polygonaceae
Oxygonum
dregeanum Meisn.
[umdambane]
Roots
Leaves
Triterpenoid saponins,
oleasterol and
flavonoids.
Abdominal pains, inflammatory
conditions, schistosomiasis,
convulsions, whooping cough,
aphrodisia, diarrhoea and snakebite.

62.50

75.00
26. Rosaceae
Rubus pinnatus
Willd.
[amakonubi]
Roots
Leaves
Polyphenolics and
tannins, terpenoids.
Coughs and other respiratory
complaints, toothaches, convulsions,
chronic diarrhoea, abdominal cramps
and rheumatism.

50.00

25.00
27. Rubiaceae
Catunaregam
spinosa (Thunb.)
Tirvengadum
[isibihla]
Roots
Leaves
Fruits
Alkaloids, iridoids,
ursolic acid-based
saponins, oleanolic acid
derivatives, triterpenoid
saponins
Epilepsy and dizziness, fevers,
aphrodisiac, headaches snakebite,
nausea, respiratory and
gynaecological ailments, rheumatism,
emesis, diuresis, schistosomiasis,
gonorrhoea and other bacterial
infections.

75.00

50.00
28. Rubiaceae
Gardenia ternifolia
Schumach. & Thonn
[umkwakwane
omkhulu]
Roots
Leaves
Twigs
Fruits

Triterpenoids and
tannins.

Malaria, protective charm against
lightning and sorcery, sore eyes,
headaches, madness, coughs,
asthma, dysmenorrhoea, infertility,
chorea, epilepsy and convulsions,
earache, schistosomiasis,
rheumatism, abdominal pains and fish
poison.

62.50

50.00
29. Rutaceae
Clausena anisata
(Willd.) Hook. F. ex
Benth.
[isifudu]
Roots
Leaves
Fruits
Sesquiterpenoids, fatty
acids, umbelliferone,
scopoletin, limonene,
alkaloids clausanitine
and mupamine,
coumarins heliettin and
chalepin, limonoids and
phenylpropanoids.
Convulsions, taeniasis and other
parasitic infections, constipation,
rheumatism, malaria and fevers, heart
ailments, bad breath, abdominal pains
and toothaches, mental diseases,
headaches, eye complaints,
impotence and sterility, battle charms.

87.50

75.00

Table 1 (Continues)

30. Sapotaceae
Englerophytum
magalismontanum
Krause
[umnugumabele]
Roots
Fruits
Ascorbutic acid, tannin,
steroids, triterpenoids,
oleanonic acid
derivatives.
Epilepsy, headaches, abdominal
pains, rheumatism and inflammatory
conditions.

75.00

62.50

31. Solanaceae
Datura stramonium
Linn.
[iloyi]
Leaves
Fruits
Aerial
Parts
Tropane alkaloids,
atropine, hyoscine, and
other atropine-like
drugs, sesquiterpenoids
Asthma, bronchitis, coughs and many
other respiratory conditions,
rheumatism, gout, boils, abscesses
and wounds, aphrodisia, motion
sickness, sore throat and tonsilitis,
visceral pains, epilepsy and
Parkinsonism.

37.50

25.00
32. Solanaceae
Withania somnifera
(Linn.) Dun.
[ubuvimbha]
Roots
Leaves
Aerial
parts

Triterpenoid saponins,
tropanol, sitoindosides,
alkaloids, choline,
steroidal lactones,
withaferine A,
withasomnine,
withanolides, and
flavonoids.
Fevers, sores, abscesses, wounds,
syphilis, skin diseases, diarrhoea,
proctitis, asthma, nausea,
rheumatism, inflammation and pain,
conjunctivitis, scabies and carbuncles,
aphrodisia, sedation,
epilepsy/convulsions.

75.00

62.50
33. Verbenaceae
Clerodendrum
glabrum E. Mey.
[umnukambiba]
Leaves
Roots

Steroidal saponins,
flavonoids, and
terpenoids.
Fevers, intestinal parasites, childhood
convulsions, colds, sore throats and
chest complaints, fractured bones,
toothaches, skin rashes, sedation and
body pains.

50.00

37.50
34. Verbenaceae
Lippia javanica
(Burm. F.) Sreng.
[umsuzwane]
Leaves
Twigs
Volatile oil,
monoterpenoids, various
organic acids and
alcohols, iridoid
glycosides and
pentacyclic triterpenoids.
Coughs, colds, bronchitis, asthma and
other chest ailments, malaria, fevers,
stomach problems and headaches,
convulsions, cataracts, diarrhoea,
scabies and body lice.

62.50

50.00
35. Vitaceae
Rhoicissus
tridentata (Linn. F.)
Wild & Drum.
[isinwazi]
Roots
Tubers
Leaves
Proanthocyanins and
flavanoids.
Epilepsy, dysmenorrhoea, safe
delivery in pregnancy, renal
complaints, menorrhagia infertility,
stomach ailments, swellings, colds,
wounds, boils and sores.

37.50

25.00

DISCUSSION AND CONCLUSION
The results of this experimental animal study
indicate that the group of Zulu medicinal plants
evaluated for anticonvulsant properties possess
weak to strong anticonvulsant effects in the
laboratory mammalian animal model used,
despite the fact that the plants belong to diverse
families, and contain different chemical
constituents. The most frequently cited families
of plants with anticonvulsant properties are
Asteraceae, Bignoniaceae, Fabaceae,
Verbenaceae, Rubiaceae, Rutaceae,
Commelinaceae, Meliaceae, Lamiaceae,
Solanaceae, Apocynaceae, Euphorbiaceae,
Myrtaceae, Polygonaceae, Rosaceae,
Crassulaceae, Sapotaceae, Capparaceae,
Vitaceae, and so forth (24). These are very large
and widely distributed plant families. The
phylogenetic distance between this select group
of plant families may be a strong indication of the
varied nature of their active chemical
constituents.

Our ethnobotanical literature survey has
revealed that 28 of these 35 (ie, 80%) medicinal
plants used in the control or management of
epilepsy/convulsions in Zulu folk medicine have
been used in traditional medicine in other parts
of the world to manage epileptic seizures. The
literature survey has also shown that although
relatively very little scientific investigations have
been undertaken to rationalise the use of the
medicinal plants examined in this study as
anticonvulsant remedies in South Africa, 21 (ie,
60%) of these Zulu indigenous anticonvulsant
remedies have had some experimental testing
for anticonvulsant activity elsewhere in the world.

A summary of our pharmacological evaluation of
the plant extracts for anticonvulsant activity
(presented in Table 1) shows that the 35
medicinal plants commonly employed in Zulu
traditional medicine as antiepileptic remedies,
produced weak to strong anticonvulsant effects
in mice. This observation probably reflects the
great variety of possible active antiepileptic
chemical compounds present in the plants. A
number of secondary plant metabolites with
diverse chemical structures have been shown to
possess anticonvulsant activities. The wide
variety of chemical compounds with
anticonvulsant properties present in the plants
examined in this study probably suggest that a
diversity of mechanisms of action must be
involved in the antiepileptic actions of the various
plant constituents. Many plants containing
complex amino acids, alkaloids, glycopeptides,
terpenoids, peptides, amines, steroids,
flavonoids, lipids, iridoids, coumarins, simple
phenolics, polyphenolics, inorganic salts,
sulphur-containing compounds, vitamins,
xanthenes, stilbenes, phenylpropanoids, or
cyanogenic glycosides have been reported to
possess antiepileptic activities (24). The
physiological importance of the plant nutrients in
balancing the chemical and biochemical
activities of epileptic patients has long been
recognised (27), and cannot be over-
emphasised. The medicinal and nutritive values
of essential and volatile oils are well documented
and clearly established in medical literature.
Essential oils such as eugenol, anethole,
chamomile, and so on, are known to have
sedative, carminative, anticonvulsant, and
antimicrobial properties. Such oils have been
identified from many plants in the
Amaryllidaceae, Labiatae, Rutaceae, and other
plant families (28). The incorporation of a large
number of plant extracts known to contain
volatile and/or essential oils in Zulu indigenous
anticonvulsant remedies tend to suggest that
such remedies will be therapeutically useful in
controlling convulsions of organic and
pathological origins.

Plants containing coumarins, steroids, vitamins
and complex carbohydrates have also been
credited with anticonvulsant actions. Coumarins
occur naturally in many plants, and have been
reported to produce anticonvulsant effects in
chemically-induced seizures in laboratory
mammals (29, 30, 31). Although the exact
mechanism of the anticonvulsant action of
coumarins is still unknown, it has been widely
speculated that it involves depression of the
CNS, like phenobarbitone and diazepam.
However, it is apparent from the above
discussion that various chemical constituents of
the plants examined in this study produce
anticonvulsant effects through many
mechanisms. The lack of perfect models for
epilepsy and/or convulsion in experimental
animals, coupled with financial restrictions on
obtaining and maintaining animals, as well as
social restrictions on extensive use of animals in
pharmacological experimentation, indicate that a
more practical approach to scientific screening of
indigenous plants for anticonvulsant activity
would involve a series of in vitro pre-testing
before examining a potential new antiepileptic
agent in laboratory animals.

The mechanism of pentylenetetrazol (ie,
metrazol-)-induced seizures is still speculative
(14). However, according to De Sarro, et al.,
(1999) (32), metrazol-induced seizures may be
due to inhibition of GABAergic mechanisms in
the brain. In the present study, the two
(reference) standard antiepileptic drugs used (ie,
phenobarbitone and diazepam) profoundly
antagonised metrazol-induced seizures in the
mammalian experimental animal model used.
Phenobarbitone and diazepam have been
reported to antagonise chemoshock seizures by
enhancing GABA-mediated inhibition of the brain
neurons (14). Since the plant extracts examined
in this study offered 12.50% to 87.50%
protections and delayed metrazol-induced
seizures, it is likely that the plant extracts exerted
their anticonvulsant actions, at least in part, via
GABAergic mechanisms. Picrotoxin has been
claimed to induce seizures by antagonising the
action of GABA on chloride ion channels.
Stimulation of GABA
A
-receptors by GABA has
been credited with the blockade of chloride ion
channels of the brain neurons. This blockade
prevents the conductance of chloride ions in the
brain neurons. In this study, phenobarbitone and
diazepam antagonised picrotoxin-induced
seizures in the mice. The plant extracts
examined also delayed the latency and offered
12.50% to 75.00% protections against picrotoxin-
induced seizures. This finding probably
strengthens the earlier proposal that the plant
extracts might have produced their
anticonvulsant effects through GABAergic
mechanisms.

Although synthetic anticonvulsant agents have
played a major role in the treatment and/or
management of epilepsy since their introduction
into clinical medicine from 1912 upwards,
serious adverse effects and economic
constraints have limited their popularity in many
communities. Questions involving their clinical
pharmacology and mechanisms of actions have
spawned an incredible amount of basic and
clinical research. Controversy regarding their
clinical efficacy and potential hazards have often
been raised and discussed. Many major clinical
questions still remain to be answered about the
drugs. It is obvious that the way forward in the
effective management of epilepsy is the
development of newer, cheaper, and safer
antiepileptic agents, possibly from higher plants.
The search for the ideal anticonvulsant agent
has been hampered mainly by a lack of
fundamental knowledge of the basic biochemical
abnormalities of epilepsy. Some of the questions
that remain to be answered include: What is the
primary lesion of epilepsy? How is the lesion
transmitted from one generation to the other?
Can it be detected in the pre-epileptic state?,
and so forth. Until the answers to these
questions and many others are found,
pharmacologists and medicinal chemists will be
forced to continue a random search for more
effective and safer anticonvulsant drugs.

It is important to appreciate, however, that there
are many plants and plant extracts which
possess marked anticonvulsant activities. From
ancient times, such plant drugs have been used
for the treatment of epilepsy, and they still find
extensive use in traditional medicine worldwide
today. Methods of evaluating anticonvulsant
agents include: (i) pre-clinical testing of their
anticonvulsant effects in chemically- and
electrically-induced seizures in experimental
animals (such as mice, rats, rabbits, and so on);
and (ii) clinical trials involving both normal
human volunteers and epileptic patients. Such
tests do not usually examine the toxicity of the
compounds. The wide range of chemical
structures of those plant constituents which
appear to be the active anticonvulsant principles
in the plant drugs examined in this study would,
therefore, probably suggest not only different
mechanisms of action, but also different sites of
action of the drugs in the body.

Paracelsus (1493-1541) (33) once stated that:
All substances are poissons, there is none which
is not a poison. The right dose differentiates a
poison from a remedy. Indigenous
anticonvulsant remedies will be more
therapeutically useful if their right doses are
known and used. The routes of administration of
indigenous remedies are also crucially important.
All indigenous anticonvulsant remedies prepared
as concoctions, decoctions, etc, are usually
taken orally, while some are used in bathing, but
NEVER administered parenterally via the needle.
The absorption, bioavalability, distribution,
biotransformation and excretion profiles of orally-
administered drugs are known to differ from
those administered by other routes, particularly
those administered parenterally. Indigenous
anticonvulsant remedies, like other crude drug
preparations containing many plant metabolites,
may exhibit interesting pharmacological
properties such as anticonvulsant, CNS
depressant, analgesic, antimicrobial,
hypotensive, anti-inflammatory, and so forth; and
may also have high nutritive values. Crude
extracts may, however, contain toxic
components or chemicals which may be harmful
to animals and man.

Scientific investigations of traditional medicines,
as in the examples provided above, have
resulted in the discovery of a number of
promising leads for new anticonvulsant agents.
While a long history of traditional use of a plant
drug may suggest that the plant is relatively non-
toxic, the safety of the herb should be confirmed
by in-depth literature search and properly-
controlled experimental bioassays. Modern drug
discovery requires a systematic approach to
optimise time and resources. It is essential to
involve traditional healers, phytochemists and
organic chemists, pharmacologists, and medical
practitioners working together to achieve the
greatest benefit from new drugs developed from
traditional remedies. With the increasing
incidence of epilepsy in both urban and rural
populations of the world, the inability of current
modern therapies to control all the metabolic
defects of the disease and their pathological
consequences, coupled with the serious adverse
effects and the enormous cost of modern,
conventional pharmacotherapeutic agents; there
is a dire need to develop new, effective,
inexpensive, non-toxic, indigenous alternate
strategies for epileptic therapy. Nevertheless, the
results of this experimental animal study have
shown that the medicinal plant extracts
examined possess weak to strong anticonvulsant
properties, and thus lend credence to the
folkloric use of the plants as antiepileptic
remedies in Zulu traditional medicine.

ACKNOWLEDGEMENTS
I am indebted to the staff of Natal Provincial
Herbarium in Durban, South Africa, and to the
staff of the Department of Botany, Faculty of
Science, University of Durban-Westville, Durban,
South Africa, for the identification of the plant
materials used in this study. The assistance of
Ms Thembisa Jikwa in the collection of some of
the plants and recipes examined in this study is
gratefully acknowledged. I am grateful to Mrs.
Patience Koloko (Director, KwaZulu-Natal
Traditional Healers Affairs) for her assistance
and interest in this study; Dr. Esther K. Mutenda
for her assistance in the extraction process;
Professor Clement O. Adewunmi for granting me
an unlimited access to the facilities in his
laboratory, and also for his constructive
criticisms; and to the Council of the University of
Durban-Westville, Durban 4000, South Africa, for
the provision of a Research Grant (R642) to
carry out a part of this study.

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anticonvulsant effects of an aqueous extract from
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Este artculo puede ser libremente distribuido y/o copiado para uso
personal siempre que lo sea en su integridad. No se permite su
modificacin ni su uso parcial o total para fines comerciales. Si por
cualquier razn Vd. desea redistribuirlo en gran cantidad le
agradeceremos que nos lo informe. Todo trabajo basado en este
artculo o derivado de su uso debe citar convenientemente la fuente.

http://www.blacpma.cl


Correspondencia

Desde Argentina

Estimado Jos Luis:
En estos momentos, por razones de trabajo slo
puedo dejar constancia de la recepcin y desear que
BLACPMA siga progresando.
Muy cordiales saludos,

Nstor Caffini
Universidad Nacional de La Plata
Editor Acta Farmacutica Bonaerense.

Desde Mxico

Estimado Jos Luis Martnez:
Le agradezco su mensaje y al mismo tiempo le
felicito por esta actividad en la que promueve la
integracin de la comunidad Latinoamricana
interesada en las plantas medicinales y aromticas y
nada mejor que un instrumento muy bien hecho
como el BLACPMA.
Cosiderar seriamente su atenta invitacin.
Atentamente

Andrs Navarrete
Facultad de Qumica,
Departamento de Farmacia,
Universidad Nacional Autnoma de Mxico.

Desde Argentina

Estimado Jos Luis:
Muchas gracias una vez ms por el Boletn. En un
futuro cercano espero poder hacer alguna
contribucin.
Muchos saludos.

Diego Estomba
San Martn de los Andes,
Argentina.

Desde Bolivia

Estimado Jos Luis Martnez:
Estoy muy agradecida por la gentileza que usted
tiene en enviarme el boletn BLACPMA, todos los
artculos son novedosos y las frases muy bien
seleccionadas, mis felicitaciones por el trabajo de
equipo.
Atentamente

Dra. Jenny Durn,
UMRPSFXCH Sucre, Bolivia

Desde Argentina

Estimado Jos Luis:
He ledo por primera vez el BLACPMA Vol.3 N 6,
gracias al reenvo de una colega y ha sido una muy
agradable ocasin para conocerlos y poder
presentarnos.
Constitumos hace exactamente un ao en forma
Oficial con Personera Jurdica 675/2003, una
ASOCIACIN de AMIGOS del MUSEO de
FARMACOBOTNICA de la Facultad de Farmacia
y Bioqumica de la Universidad de Buenos Aires,
por ello nos interesa muy especialmente recibir en el
2005 este Boletn para difundirlo entre nuestros
Asociados y para hacerles llegar las informaciones
relativas a las actividades que se llevan a cabo en el
Museo de Farmacobotnica "Prof. Dr Juan A.
Dominguez, bajo la Direccin del Prof. Dr J. L.
Amorin.
Lo saluda cordialmente

Ruth Galperin de Levy.

Desde Colombia

Estimado Jose Luis:
Recib la edicin del Boletn del mes de Noviembre.
Una vez ms lo felicito por su esfuerzo en la difusin
de las investigaciones realizadas en las plantas
medicinales.
Un caluroso saludo.

Jhon J. Rojas
Docente, Universidad de Antioquia.

CORRESPONDENCIA (sigue)

Desde Argentina

Estimado Jose Luis:
agradezco el envo del Boletn N 6. Me parece muy
interesante el artculo del acceso a los recursos
naturales de Chile. Felicidades por los logros y
adelantos.
Abrazos,

Ana H. Ladio,
Universidad Nacional del Comahue, Centro Regional
Universitario Bariloche, Departamento de Ecologa
Quintral 1250-8400- San Carlos de Bariloche, Ro
Negro, Argentina.

Desde Colombia

Hola Jose Luis:
acuso recibo del Vol. 3 N 6 de BLACPMA....saludos,
felices fiestas y prospero ao para los tuyos y a todos
los integrantes del BLACPMA,
atentamente,

Ivan Corts,
Administrador web-site:
www.asociacioncolombianadecienciasbiologicas.org
Universidad del Quindo, Armenia.

Desde Per

Estimado Dr. Jose Luis Martnez:
debo agradecerle por el envo del Boletn BLACPMA del
mes de Noviembre y as mismo felicitarlo a Ud. y a su
equipo por la labor realizada, as mismo reconocer la
ayuda que nos brinda con informacin precisa con
respecto a plantas medicinales y de los eventos
relacionados al tema que se realizan. Deseando que se
cumplan todas sus metas para el 2005 quedo de Ud.

Len Villegas,
Departamento de Ciencias Farmacuticas,
Facultad de Ciencias y Filosofa,
Universidad Peruana Cayetano Heredia.

Desde Argentina

Estimado Jos Luis:
acuso recibo del BLACPMA Vol. 3 N 6. Considero que
el mismo esta llegando a niveles de altsimo inters.
Muchas gracias por tu esfuerzo.

Rita Ins Zeichen,
ANMAT, Buenos Aires, Argentina.

Desde Nicaragua

Estimado Jos Luis:
Gracias por el mensaje. Te felicito por la constancia y el
esfuerzo para seguir adelante con el Boletn. Slo he
podido darle una lectura superficial y me parece bien. Si
tengo ms comentarios te los har llegar.
Abrazos,

Ernesto Medina Sandino,
Rector, Universidad Nacional de Nicaragua,
(UNAN-Len).

Desde Bolivia
Estimado Jos Luis:
Una vez ms te agradezco la amabilidad de enviarnos la
revista, te deseo mucho xito.
Un cordial saludo.

Gloria Saavedra,
Centro de Tecnologa Agroindustrial, Universidad Mayor
de San Simn, Cochabamba, Bolivia.

Desde Chile

Hola Jos Luis:
recib BLACPMA Vol.3 N 6 - Noviembre 2004. Gracias.
Como siempre, muy interesante para los que valoramos
las virtudes de la naturaleza.

Claudia Bjar,
Santiago, Chile.

Desde Venezuela

Estimado Jos Luis:
La presente es para confirmarle que recib el ltimo
nmero de la Revista electrnica, y adems felicitarle y
expresarle mi satisfaccin al encontrar mi nombre en la
parte de correspondencias recibidas, realmente es una
buena estrategia para que los investigadores de esta
rea se sientan motivados a revisar la Revista y emitir
sus comentarios. Solo me queda decirle que continen
trabajando y mostrando al mundo que pese a nuestras
limitaciones en Latinoamrica tambin se
hace investigacin....., carios, desde Mrida,
Venezuela,

Judith Josefina Velasco,
Facultad de Farmacia y Bioanlisis,
Universidad de los Andes.

Frases y citas

El arte de la medicina consiste en mantener
al paciente en buen estado de nimo
mientras la naturaleza le va curando.

Voltaire

Temor por un padre no significa
necesariamente respeto por l

Lord Robert Baden Powell

Cuide a su jefe, el prximo puede ser peor

Julio Lobos

Solo podemos amar aquello que
conocemos y solo podemos proteger
aquello que amamos

Tobas Lasser

Casi todos podemos soportar la
adversidad, pero si quieres probar el
carcter de un hombre, dadle poder

Abraham Lincoln

Las palabras sin afectos, nunca llegarn a
oidos de Dios

William Shakespeare

Mucho sabra, en verdad, si supiera la
razn donde acaba la ilusion y comienza la
realidad

Ramn de Campoamor

Cuando la suerte sonrie que necesidad
hay de tener amigos?

Eurpides

Dos clases de hombres se esfuerzan en
vano: quien amontona dinero sin gastarlo y
quien adquiere saber sin aplicarlo

Saadi

El hombre tiene mil planes para si mismo.
La suerte, solo uno para cada uno.

Aristoteles

Prefiero las personas a los
principios y, sobre todo, prefiero a
las personas sin principios

Oscar Wilde

Un oficio esta bien hecho, cuando
cualquier imbecil lo entiende

Humberto Silva

Ensear es muy fcil
Educar es muy dficil

Alberto Hurtado

Los hechos no dejan de existir
porque se los ignore

Aldous Huxley

Queris conocer a un hombre?
Investidle de un gran poder

Pitaco

Mejor una mala excusa que ninguna

William Canden

La suerte de la fea,
la bonita la desea

Gregorio Lunetto

Mdicos. Hombres de suerte.
Sus xitos brillan al sol
y sus errores cubren la tierra

Michel E. de Montaigne

Mi libertad consiste en tomar de la
vida lo que me parece mejor
para m y para todos;
y en darlo con mi vida.

Juan Ramon Jimenez

No cambies la salud por la riqueza,
ni la libertad por el poder.

Benjamin Franklin
B
B
L
L
A
A
C
C
P
P
N
N
A
A

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BOLETIN LATINOAMERICANO Y DEL

CARIBE DE PLANTAS MEDICINALES Y

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