“THE USE OF HERBAL MEDICINE IN THE TREATMENT OF PARKINSON’S DISEASE”: A

CASE STUDY OF NONOTHORDOX MEDICINAL PRACTITIONERS AT AMUWO-ODOFIN

LOCAL GOVERNMENT AREA, LAGOS STATE.
AISIEN CHUKWUDUMEBI MARY
BEING A RESEARCH PROJECT SUBMITTED IN PARTIAL FULFILMENT FOR THE AWARD
OF PROFESIONAL BSC IN NATUROPATIC MEDICINE SUBMITTED TO THE
DEPARTMENT OF NATUROPATIC MEDICINE, HAVILAH NATURAL MEDCINE NIGERIA.

SUPERVISOR

DR ADEMOLA BANKKADEJO NNDDO FCPNM

ACKNOWLEDGEMENT
ALL PRAISES AND ADORATION BELONGS TO JESUS, THE BEGINNING AND END, THE GREATEST
PHYSICIAN . THE ONE WHO KNOWS IT ALL!

I APPRECIATE THE SUPPORT AND ENCOURAGEMENT OF MY HUSBAND AISIEN ROTIMI, FAMILY

AND FRIENDS, MY FELLOW COLLEGES AND LECTURERS FOR THEIR ASSISTANCE AS WELL .
 ABSTRACT
Parkinson's disease is a multifactorial disorder of the nervous system in which there
is a progressive loss of dopaminergic neurons. There is a disturbance in the
movement in Parkinson's disease and these include resting tremors, rigidity,
bradykinesia or akinesia, disturbance, posture and freezing (motor block). The
substantia nigra and other parts of the brain are commonly affected. The disorder
could be related to oxidative stress and there is an important role of reactive oxygen
species. A number of herbal plants contain active components which are known to
treat Parkinson’s disease. Hence, the potential role of herbal plants in treating
Parkinson's disease cannot be undermined. In the present narrative review, the main
aim is to discuss twenty two (22) plants which were found to be useful for the
treatment of Parkinson’s diseases but the most prominent among these plant
families are Musaceae Curcuma longa (Zingiberaceae), Juglandis Semen (asala)
(Walnut), Nicotina tabacum Linn(ewe taba)(tobacco leaves), Mucuna pruriens
(werepe) (Velvet bean)and Piperaceae (Atareaja Seed)some having two species each.
The leaves constitute the most frequently used parts. Other parts such as root, fruit
and stem bark are occasionally used. The modes of preparations are infusion,
decoction and concoction which are administered orally, mostly three times daily.
Most of the herbs are sourced from the wild; only a negligible number of
practitioners have home gardens where plants are grown. It is therefore imperative
to encourage the cultivation and proper documentation of some of the plants which
may become endangered over long use.
CHAPTER ONE
1.1 BACKGROUND OF THE STUDY

Parkinson’s disease was first described by James Parkinson in 1817 under the term
“the shaking palsy”, and later named to his honor. Parkinson’s disease is a type of
movement disorder that can affect the ability to perform common, daily activities.
Although Parkinson’s disease is associated with a wide range of symptoms, there are
features of Parkinson’s disease that most people with the condition will experience.
These symptoms are typically divided into those that affect movement (motor
symptoms) and those that do not (non-motor symptoms). The most common motor
symptoms of Parkinson’s disease are tremor (a form of rhythmic shaking), stiffness or
rigidity of the muscles, and slowness of movement (called bradykinesia). A person
with Parkinson’s disease may also have trouble with posture, balance, coordination,
and walking. Common non-motor symptoms of Parkinson’s disease include
constipation, anxiety, depression, fatigue, pain, tingling, hyposmia, sleep disturbance,
and cognitive impairment among others. It is important to note that, although there
are common symptoms of Parkinson’s disease, they can vary greatly from person to
person. Moreover, how these symptoms change over time and whether other
symptoms of Parkinson’s disease emerge differ from person to person. Most people
who develop the symptoms of Parkinson’s disease do so sometime after the age of
50, but Parkinson’s disease can affect younger persons as well. There are an
estimated 598,000 in Nigeria living with Parkinson’s disease, 1 million Americans and
more than 10 million people worldwide.

Parkinson’s disease is a neurodegenerative disease with the pathological hallmark of

Parkinson’s disease a loss of dopaminergic neurons (nerve cells) in certain areas of
the brain, including a region called the substantia nigra (sub-STAN-she-uh NYE-gruh),
Latin for “black substance.” The neurons in this region (which appear dark under a
microscope) produce a neurotransmitter (a chemical messenger that allows neurons
to communicate) called dopamine. Dopamine helps to regulate movement. As the
number of cells in the substantia nigra decreases, there is less dopamine available in
the brain. Dopamine is important to maintain normal movement patterns. This loss
of dopamine is the reason that many treatments for Parkinson’s disease are intended
to increase dopamine levels in the brain. Loss of neurons in other parts of the brain
also occurs in Parkinson’s disease, and accounts for some of the non-motor
symptoms of the disease. In addition to decreases in dopamine and the cells that
make dopamine, you might also read or hear about a protein called alpha-synuclein
(AL-fa-sin-NUKE-lee-un). Studies suggest that alpha-synuclein normally helps neurons
communicate with each other. In Parkinson’s disease, the protein clumps up in
microscopic aggregates called Lewy (LOOee) bodies. Researchers believe that alpha-
synuclein build-up contributes to the development of Parkinson’s disease, and that
developing treatment that reverses this build-up will make a great difference for
which the timeline remains unclear making Parkinson’s disease the second most
common neurodegenerative disease in the world. Current conventional treatment
for Parkinson’s disease is based on the dopamine replacement therapies and
reduction of dopamine degradation, including levodopa, dopamine receptor
agonists, monoamine oxidase-B inhibitors, catechol-O-methyltransferase inhibitors
and other types of drugs (Rogers et al., 2017). However, all the current therapeutic
approaches remain palliative and can't inhibit or reverse the progression of
Parkinson’s disease (Athauda and Foltynie, 2015). Furthermore, frequently with
these treatments can lead to obvious adverse events and efficacies diminished, as
well as induce therapy-related motor complications such as dyskinesia,
choreoathetosis, and fluctuations in motor function (Jenner, 2015). A safer and more
effective alternative treatment of Parkinson’s disease is increasingly demanded.
The herbal medicine, therapy for Parkinson’s disease has become particularly a
common intervention in most Countires like China, which could be traced to the
Huangdi Neijing (Inner Canon of Yellow Emperor) (Zheng, 2009), the earliest existing
classics in Chinese herbal medicine. Up to now, herbal medicine is still very popular in
the treatment of Parkinson’s disease especially in Asian countries (Wang et al.,
2011, 2013) although Previous reviews (Wang et al., 2012; Zhang et al., 2015) found
lack of evidence of supporting the use of herbal medicine for Parkinson’s disease
patients because of the generally low-quality studies included. Here in Nigeria it is
known that Nigeria is one of the most important countries in West Africa richly
blessed with great diversity of medicinal plants. However, some of these plants are
becoming threatened and endangered (Sonibare and Abegunde, 2012). Hence, there
is the need to document and research into various medicinal plants used in treating
diseases in different parts of Nigeria. Ethnobotanical surveys of patrkinson’s diseases
in the Southwestern part of Nigeria similar to the one presented in Amowo-odofin
Local Government Area, Lagos State.

Definition:
The golden standard for a definite diagnosis of Parkinson’s disease relies on the
typical clinical presentation combined with a post-mortem histopathology
confirmation of characteristic neuronal loss and presence of LBs. Functional brain
imaging [e.g., dopamine transporter imaging combined with single-photon emission
computed tomography] cannot distinguish Parkinson’s disease from other
degenerative causes of parkinsonism (e.g., PSP, MSA, CBD, and DLB), but is of value
to differentiate against, e.g., essential tremor, drug induced tremor, and psychogenic
symptoms. Structural brain imaging methods, such as magnetic resonance imaging,
are also of value to rule out some differential diagnoses, e.g. vascular Parkinsonism.
Still, due to the lack of specific biomarkers, Parkinson’s disease is in practice a clinical
diagnosis. To assess and describe the severity of Parkinson’s disease, several clinical
scales have been developed. The most traditional example is the Hoehn and Yahr
scale, first introduced in the 1960’s and since then used worldwide in clinical
research as the standard staging system for Parkinson’s disease as shown in Table1.
The original version includes the 5stages defined by hallmarks such as bilateral
involvement (stage 2) and impaired postural reflexes (stage 3). A modified version
has later been introduced, with the addition of intermediate stages between the
original 5. The Hoehn and Yahr scale was developed in the era before dopaminergic
replacement therapy was available, and is only descriptive; the authors did not
presume a sequential stage-to-stage progress of disease. The setup of hallmarks
categorizing each stage in the Hoehn and Yahr scale is somewhat ambiguous, as
clinical signs and functional impairment may occur in combinations that diverge from
the criteria of each stage. As for evaluation of disease progress and treatment
effects, more detailed scales have later been developed, commonly validated with
the Hoehn and Yahr scale as the reference
Table 1. original and modified Hoehn & Yahr scale

Hoehn & Yahr scale Modified Hoehn & Yahr scale

1.0: Unilateral involvement 1.0: Unilateral involvement only
only, usually with
minimal or no
functional impairment.
1.5: Unilateral and axial
involvement
2.0: Bilateral or midline 2.0: Bilateral involvement
involvement, without without impairment of
impairment of balance. balance
2.5: Mild bilateral disease with
recovery on pull test
3.0: First sign of impaired 3.0: Mild to moderatebilateral
grihting reflexes. This is disease; some postural
evident by unsteadiness instability; physically
as the patient turns or is independent
demonstrated when he
is pushed from standing
equilibrium with the feet
together and eyes closed.
Functiionally the patient
is somewhat restricted
onally
in his activities but may
have some work
potential depending
upon the type of
employment. Patients
are physically capable of
leading independent
lives, and their disability
is mild to moderate.
4.0: Fully developed, 4.0: Severe disability; still able
severely disabling to walk or stand unassisted
disease; the patient is
still able to walk and
stand unassisted but is
markedly incapacitated.
5.0: Confinement to bed or 5.0: Wheelchair bound or
wheelchair unless aided. bedridden unless aided
The prevalence of Parkinson’s disease show that more than 10 million individuals
affected worldwide and almost 598,000 in Nigeria, PD is the second most common
neurodegenerative disease. Men are at about 50% higher risk than women. The
incidence is strongly related to age, but approximately 30% of the patients are
younger than 50 years of age at the time of diagnosis. The terms “early onset” or
“young onset” are commonly used with a cut-off age at 40 or 50 years higher.
There are increased physical and psychological morbidity effects on the quality of life
associated with the following complications of Parkinson’s disease:
A. Bradykinesia
B. Tremor
C. Rigidity
D. Postural and gait impairments
E. Autonomic dysfunction
F. Cognitive and neuropsychiatric features
G. Sensory dysfunction
H. Sleep disorders
I. Fatigue
J. Pain
K. Dyskinesia
L. Hallucinations
M. Impulsive control disorders

1.2 STATEMENT OF THE PROBLEM

With more than 10 million individuals affected worldwide, and almost 598,000 in
Sweden, Parkinson’s disease is the second most common neurodegenerative disease.
Men are at about 50% higher risk than women. The incidence is strongly related to
age, but approximately 30% of the patients are younger than 55 years of age at the
time of diagnosis. The terms “early onset” or “young onset” are commonly used with
a cut-off age at 40 or 50 years
There are many risk factors associated with Parkinson’s disease which are; trauma,
emotional stress, personality (shyness and depressiveness), diets, toxicity of Metals
(manganese, iron), Drinking of well water, farming, rural residence, wood pulp mills,
steel alloy industries, herbicide and pesticide exposure, MPTP and MPTP-like
compounds, Female cleaners. The major risk factors are age, environment

Modifiable risk factors

Exposure to chemicals is also a risk factor where people who work in certain
professions may have a higher chance of developing Parkinson’s disease because of
exposure to certain chemicals are toxic with some evidence that exposure to certain
toxins can increase the chance of developing Parkinson’s disease, according to the
Parkinson's Foundation, Herbicides and pesticides, these may include; paraquat,
fungicides, such as maneb, insecticides such as rotenone be it colorless or odorless ,
pesticides chemicals that were present in the defoliant Agent Orange which was used
in the Vietnam War, have been linked to Parkinson’s disease, although scientists have
not definitively proven the link. Studies have suggested that there is a higher rate of
Parkinson’s disease among people who work as farmers, those who are exposed to
well water, and those who live in the countryside. Although more studies are
necessary to confirm any precise links, researchers believe that exposure to toxins,
such as pesticides, increases the risk.

Researchers have noted a link between long-term exposure to certain metals and a
higher risk of Parkinson’s disease. The metals that might do this are: mercury, lead,
manganese, copper, iron, aluminum, bismuth, thallium and zinc. However, the risk is
difficult to measure, and there is no evidence to confirm an exact that any of these
metals specifically pose this type of hazard. Medications and other drugs which are
antipsychotics for treating severe paranoia and schizophrenia, synthetic heroin
product, MPTP — can also cause Parkinsonism or Parkinson-like symptoms
In April 2018, scientists published notes on case studies of seven young adults who
had used the drug. The individuals showed symptoms of Parkinsonism after short-
term use of the drug.

Non-modifiable risk factors

Genetic factors and family history is a risk factor. A person who has a close relative —
such as a sibling or parent — with Parkinson’s disease has a slightly higher risk of
developing it, compared with others. According to the Parkinson's Foundation,
around 10 to 15 percent of cases are probably due to hereditary genetic factors. The
others are "sporadic." There is currently no way to predict that they will occur.
Head trauma is another risk factor. People who receive a blow to the head at least
on one occasion may have a higher chance of developing Parkinson’s disease.
A study published in 2018 found that, among military veterans, even a mild traumatic
brain injury (TBI) can increase the risk of Parkinson’s disease by 56 percent, even
after taking psychological and other factors into consideration. This link has raised
concerns among sporting associations, as concussion is a common injury in football
and many other activities.

Two unavoidable factors that affect the risk of having Parkinson’s disease are
increasing age and whether a person is male or female.
Age: in most people who have Parkinson’s disease, symptoms become noticeable at
the age of 60 years or over.
 However, in 5–10 percent of cases they appear earlier. When Parkinson’s disease
develops before the age of 50 years, this is called "early onset" Parkinson’s disease.

Men appear to have a 50-percent higher chance of developing PD than women.

However, at least one study has found that, as women get older, their chance of
developing it increases.

Researchers have suggested that this could be due to a variety of factors, including:

 lifestyle exposures

 genetic features

 hormonal and reproductive factors

 differences in the brain structures that relate to the production of dopamine

Simply getting old is a risk factor for cardiovascular disease and risk of stroke doubles
every decade after the age of 55 yrs.
Family history of cardiovascular disease is also a risk factor. If a first-degree blood
relative has had coronary heart disease or stroke before the age of 55 years (for a
male relative) or 65 years (for a female relative) the risk increases.
Gender is significant: as man are at greater risk of heart disease than a pre-
menopausal woman. But once past the menopause, a woman’s risk is similar to a
man’s. Risk of stroke is similar for men and women.
High blood pressure can lead to hypertension complication in other parts of the body
because of the damage to the blood vessels and excessive pressure on the artery
walls can damage vital organs.
1.3 AIMS AND OBJECTIVES OF THE STUDY
- Having various herbal remedies that can assist in the treatment of Parkinson’s
Disease.
- To examine all the plant and the plant parts used for treating Parkinson’s

disease in Amuwo-Odofin Local Government Area, Lagos State.

- Determine the medicinal values these indigenous medicinal plants have in

preventing physical and psychological morbidity complications.

1.4 RELEVANT RESEARCH QUESTIONS

1. What is Parkinson’s disease?
2. What are the symptoms and signs Parkinson’s disease?
3. Are there any herbal treatment for Parkinson’s disease?

1.5 SIGNIFICANCE OF THE STUDY

The knowledge of Parkinson’s disease and the research on this remedy is significant
in order to assist people living with Parkinson’s disease live better lives as not to
alleviate the situation to a point of no solution because with many conditions that
can have both genetic and environmental causes; it may be neither one nor the other
that produces symptoms.
The higher the climb in the stages of Parkinson’s disease and the longer it goes
uncontrolled, the greater the damage. Uncontrolled Parkinson’s disease can lead to
complications including:

1. Bradykinesia
2. Tremor
3. Rigidity
4. Postural and gait impairments
5. Autonomic dysfunction
6. Cognitive and neuropsychiatric features
7. Sensory dysfunction
8. Sleep disorders
9. Fatigue
10. Pain
11. Dyskinesia
12. Hallucinations
13. Impulsive control disorders
1.6 SCOPE OF THE STUDY

This research work is intended to reveal more on the use of herbal medicine in the
treatment of Parkinson’s disease through the eyes of non-orthodox medicinal
practitioners in Amuwo-Odofin Local Government Area, Lagos State by interviewing
over 600 NONOTHORDOX MEDICINAL PRACTITIONERS comprising of traditional
medicine practitioners, herbalists, herb sellers and the elderly to encourage the
cultivation and proper documentation of some of the plants which may become
endangered over long use

1.7 LIMITATION OF THE STUDY

The research work is limited to traditional medicine practitioners, herbalists, herb
sellers and the elderly (male and female) of about age 21 and above with a limited
amount of time .

CHAPTER TWO

LITERATURE REVIEW
2.0 Introduction
This chapter gives an insight into various studies conducted by outstanding
researchers, as well as explained terminologies with regards to the challenges of
contraceptive method in Nigeria. The chapter also gives a resume of the history and
present status of the problem delineated by a concise review of previous studies into
closely related problems.
2.1.0 The potential role of herbal products in the treatment
of Parkinson’s disease

Parkinson’s disease (PD) is a neurodegenerative disease, which was first described in

1817 by James Parkinson as a syndrome of multiple physical signs such as
bradykinesia/akinesia, rigidity, postural disturbances and tremors.
The disturbance in the movement of PD is thought to becaused by the
progressive depletion of nigrostriatal neurons (located in the substantia nigra (SN) of
the brainstem), which commonly use dopamine (DA, chemical transmitter) to
communicate with other cells in the basal ganglia. However, changes are not only
restricted to the SN and may be present in other parts of the brain, as well. Therefore
depletion of DA from synaptic terminals in different parts of basalganglia is mainly
responsible for the onset of classical motor symptoms such as rigidity,
bradykinesia, and tremors. In PD, motor symptoms are usually associated with a
series of non-motor symptoms such as hyposmia, sleep disorders and depression.
Some early non-motor symptoms, such as depression or hyposmia, might refer to the
preclinical stages of PD which occurs before the onset of motor symptoms. This may
support the fact that, the site of the neurodegenerative process in PD is not only
confined to the SN. Epidemiology and prevalence of PD there are no defined or
specific methods for the diagnosis of PD. However, it is estimated that around 1
million people in the USA and 120,000 in the UK suffered from PD and the
incidence is expected to rise in the future with newly discovered advanced
diagnostic tools. Numerous studies found that the worldwide prevalence of PD
was approximately 0.3% in the general population of 40-years or above. This
prevalence rate suggests that there are 7.5 million people all over the world suffering
from PD. The average age of onset of the disease is 60-years-old, but in the case of
young-onset PD, the onset occurs between 20- and 40-years-old. The risk to develop
PD in men is about 1.5 times greater than the risk in women. The estimated PD
mortality rate is between 1.5 and 2.4. The disease itself is not the main cause of
death. However, PD patients usually die from complications like infections.
Neuroanatomy, physiology of basal ganglia and nigrostriatal pathways The basal
ganglia is a group of nuclei that includes the SN, corpus striatum (caudate and
lentiform nuclei), globus
pallidus (GP), subthalamic nucleus (STN), and thalamus.
The basal ganglia receive an excitatory input from the pre-rontal motor area,
amygdaloid nucleus, and hippocampus, mediated by the neurotransmitter glutamate.
Neurons in the SN pars compacta (SNc) release DA into to the striatum and they
control the striatal output. The striatal output system is mediated by the inhibitory
neurotransmitter gamma-amino-butyric-acid (GABA). There are five DA receptors
(D1-D5) that have been recognized; they are found in the basal ganglia and limbic
system. The D1 and D2 receptors are highly concentrated in the striatum and are
the most related to the pathophysiology of PD because they are activated by the
dopaminergic pathway originating in the SNc and terminating in the caudate and
putamen.
2.1.1Pathophysiology of PD
There are two major output pathways from the striatum: the indirect pathway
which is mediated through DA’s inhibitory influence on striatal D2 DA receptors.
In this pathway, the striatum projects to the neurons in the lateral GP (GPe)
mediated by GABA, and the GPe in turn projects to the STN, which provides
excitatory input by glutamate to the internal segment of the GP (GPi) and SN pars
reticulata (SNr). GPi and SNr have an inhibitory influence on thalamus which
suppresses thalamocortical-spinal pathway, manife-sted clinically by rigidity and
bradykinesia; then the direct pathway is mediated through DA’s excitatory influence
on striatal D1 DA receptors. The deficiency of DA decreases the inhibitory effect of
striatum on GPi and SNr. While the definite cause and mechanism of PD is still
unknown, remarkable progress has been made in understanding the underlying
mechanisms of the disease. This was achieved by new discoveries regarding the
anatomy and functions of the basal ganglia, pathological and chemical abnormalities
in PD, and by studies of genetics and experimental forms of PD. In this review, we
discuss the pathogenesis of the PD along with the role of different natural herbal
medicine in the management of the disease and their mechanisms of action.
2.1.2Pathogenesis of PD
In PD, the major MS, are related to dysfunction of cortico-striatal pathways
caused by progressive degeneration of dopaminergic neurons in the nigrostriatal
pathway. A neurodegeneration in the nigrostriatal pathways was detected by
magnetic resonance diffusion tensor imaging. Microstructural damage to frontal
and parietal lobes was detected in early onset PD which was associated with postural
and gait disturbances. Also, nigrostriatal fibers have shown that the radial variations
in this tract are related to the degree of movement disorders in PD patients. All
previous studies suggest that the neurodegeneration in the nigrostriatal pathway
plays an important role in the onset of PD symptoms. The neuronal degeneration in
PD could be explained through several theories. Collectively, we can say that
seven main factors may contribute to the neurodegeneration in PD discovered
mechanisms of the neuronal degeneration from available data sources. These include
apoptosis, immunological mechanism, proteolysis defects, oxidative stress,
mitochondrial dysfunction, iron metabolism disorders, and protein misfolding.

2.1.3 Apoptosis
It has been reported that apoptosis plays a major role in PD development. Apoptosis
is known as programmed cell death which is caused by lysosomal degradation of the
cell in a specific time followed by condensation of cytoplasm and DNA fragmentation
into apoptotic bodies. Only 0.5% of SN neurons in normal brains undergo
apoptosis, but in the case of PD, the number of neurons undergoing apoptosis is
increased up to 2% . Few studies claim that apoptosis is the main mechanism of
neuronal degeneration in PD.
Immunological mechanism the immune reactions might explain a part of PD patho-
genesis as shown by multiple studies, which tried to detect the relationship between
various pro-inflammatory cytokines and PD. An animal study showed that
Cyclooxyge-nase-2 (COX-2) appears to be up-regulated in mice models of PD. On the
other hand, the same study found out that, inhibition COX-2 prevents the formation
of potentially toxic DA-quinones and decreases the risk PD. Another study has
illustrated that T lymphocytes infiltration caused a severe damage to the neuronal
cells in PD. Proteolysis defects of Non-functional and abnormal proteins are removed
by three mechanisms: the autophagy-lysosomal pathway, the ubiquitin-proteasome
system, and molecular chaperones. α-synuclein protein (a protein that is abundant
in the human brain) is mainly removed through the previous mechanisms. Inhibition
of those mechanisms leads to accumulation of abnormal proteins that can misfold,
aggregate, and block the normal molecular pathways, leading to cell death. Parkin,
Pink1, and DJ-1 proteins form a complex that promotes degradation of misfolded
proteins and their mutations lead accumulation of abnormal proteins which may
result in features of PD . Furthermore, down-regulation of Atp13a2 gene expression
(agene that encodes a member ATPases family which transports cations) can
cause lysosomal dysfunction and increase the accumulation of α-synuclein in
vitro.

2.1.4 Oxidative Stress

Production of reactive oxygen species (ROS) may lead to neurodegeneration of
nigrostriatal neurons. DA is normally metabolized by auto-oxidation to neuromelanin
which appears to have a major role as neuroprotective, preventing toxic
accumulation of metabolites of catecholamines and removing other oxidants.
However, these metabolic pathways may produce hydrogen peroxide and
superoxideanions through interaction with membrane lipids causing toxic lipid
peroxidation, which has been reported to be abundant in the SN of PD cases.
Mitochondrial DysfunctionThe meperidineanalog: 1-methyl-4-phenyl1,2,3,6-
tetrahydropyridine (MPTP), which is a prodrug that causes permanent symptoms of
PD by destroying dopaminergic neurons in the SN of PD animal models, was used to
explain the role of mitochondria in the pathogenesis of PD. MPTP produces 1-methyl-
4-phenylpyridium (MPP
+) toxin which inhibits mitochondrial activity and stimulates endoplasmic reticulum
stress, leading to cell damage. It has been reported that mitochondrial activity was
lowered by 32 to 38% in the SN of patients with PD. Another supportive study has
shown that the lipophilic pesticide rotenone is a potent inhibitor of mitochondrial
complex I which explains the mechanism of some pesticides in the development of
PD and the role of mitochondria in understanding the mechanism. The study
included continuous administration of rotenone to rats which caused a
degeneration of the nigrostriatal dopaminergic pathway, presented clinically as
bradykinesia and rigidity.
Iron metabolism disorders elemental iron is essential for the synthesis of many
neurotransmitters including DA. It is increased by about 50% in the SN of PD
brains compared to controls which support that; abnormal iron metabolism may
play a critical role in the development of PD. A supportive study found that mice have
developed Parkinsonism due to toxic iron accumulation. Iron chelators have been
proven to prevent experimentally-induced degeneration of nigrostriatal neurons.
Protein misfolding (α-synuclein protein)Abnormalα-synuclein protein is considered as
one of the most accepted theories as for the cause of death of ni-grostriatal neurons
in PD. α-synuclein is an abundant protein located in the central nervous system. Its
function is not fully understood. However, it appears to be involved in synaptic
function . Mutations in the α-synuclein gene may cause the unfolded α-synuclein
protein to change its structure and aggregate, which interfere with nor αmal
metabolic pathways in the cell. Misfolding of proteins and formation of insoluble
aggregates can occur due to either gene mutations or aging. Lewy bodies
(intracellular inclusion bodies that are considered the pathologic hallmark of PD) are
actually an aggregated α-synuclein proteins. An animal study has shown that a single
injection of synthetic misfolded α-synuclein fibrils protein into a mouse model
resulted in progressive loss of dopaminergic neurons in the SN and motor
disturbance. α-synuclein oligomers can disrupt cell membranes of DA vesicles and
mitochondria. Diagnosis of PD till date, there are no definitive or specific
investigations for confirmed diagnosis of PD. However, it is diagnosed mainly by the
clinical features including the cardinal motor features mentioned earlier. Early
diagnosis of PD could be challenging as the signs and symptoms may overlap with
signs and symptoms of other syndromes

2.2 An evaluation of neuropsychiatric symptoms in Parkinson's disease patients

b-Saharan Africa (SSA) is composed of Afri-

can countries south of the Sahara and consists of 47
politically distinct states. SSA is one of the fastest
growing regions of the world, with significant eco-
nomic growth in the past 10–15 years, which has re-
ected in a greater availability of and access to health
facilities. However, most countries in the region are
still below the World Health Organization (WHO)
-
amined the availability of and access to evidence-
based quality care for people living with PD in SSA
countries.
is review aims to accomplish the following:
1) Provide a descriptive summary of all epidemi-
ologic and genetic studies from SSA published up
to May 2016.
2) Compare the genetic and epidemiologic re-
sults from SSA to those from other populations in
Africa outside SSA.
3) Review the level of care available and accessi-
ble to PD patients in SSA
Parkinson's disease (PD) is a chronic, progressive, and neurodegenerative disease
which may present with complaints of tremor, bradykinesia, rigidity, and postural
imbalance. Besides motor symptoms, neuropsychiatric symptoms such as depression,
hallucination, anxiety, sleep disorders, and psychosis are often encountered in
affected individuals. In a study of 139 PD patients over a 4-year observation period,
61% had at least one psychiatric symptom, while 45% had two or more psychiatric
symptoms. In the aforementioned study, depression was the most common
neuropsychiatric symptom with hallucinations, whereas anxiety was seen less often.
Vegetative, affective, and cognitive dysfunction symptoms often seen in PD may
mask depression symptoms and pose several challenges in the estimation of the
frequency of depression in PD. Therefore, different results are found in different
community-based studies on the frequency of PD. Furthermore, rates varying from
4% to 75% have been reported in several studies evaluating the frequency of
depression in PD.

Psychosis is also common in PD. Risk factors include dementia, cognitive impairment,

>65 years of age, prolonged disease duration, presence of sleep disorders,
depression, visual disturbances, and the use of drugs to treat motor symptoms of PD.

In this study, we aimed to evaluate the neuropsychiatric symptoms caused by

depression and to assess positive and negative psychotic symptoms in early and late
stage PD without dementia.

Sub-Saharan Africa (SSA) is composed of Afri-

can countries south of the Sahara and consists of 47
politically distinct states. SSA is one of the fastest
growing regions of the world, with significant eco-
nomic growth in the past 10–15 years, which has re-
ected in a greater availability of and access to health
facilities. However, most countries in the region are
still below the World Health Organization (WHO
2.3 Frequency of cognitive impairment and depression in Parkinson's disease: A
preliminary case-control study
ub-Saharan Africa (SSA) is composed of Afri-
can countries south of the Sahara and consists of 47
politically distinct states. SSA is one of the fastest
growing regions of the world, with significant eco-
nomic growth in the past 10–15 years, which has re-
ected in a greater availability of and access to health
facilities. However, most countries in the region are
still below the World Health Organization (WHO)
amined the availability of and access to evidence-
based quality care for people living with PD in SSA
countries.
is review aims to accomplish the following:
1) Provide a descriptive summary of all epidemi-
ologic and genetic studies from SSA published up
to May 2016.
2) Compare the genetic and epidemiologic re-
sults from SSA to those from other populations in
Africa outside SSA.
3) Review the level of care available and accessi-
ble to PD patients in SSA
Non-motor symptoms (NMS) of Parkinson disease (PD) are now recognized as being a
common but often overlooked feature of the disease, which can impair quality of life
and adversely affect long-term outcome.  Although some of the NMS occur as late
sequelae, they may antedate the onset of the hallmark motor abnormalities -
bradykinesia, tremors and rigidity. The NMS include olfactory and sleep disorders,
mood disorders (anxiety and depression), dysautonomia, and cognitive impairment
(including dementia).

Although both depression and cognitive impairment have been found to be common
in PD, the reported frequencies have varied widely due to methodological differences
(including the instruments). Also, the populations under study have varied, and this
may contribute to the divergent figures reported in literature. There are few reports
on the impact of depression and cognitive impairment in PD in Africans and Nigerians
specifically.

In a systematic review of 27 studies, the prevalence of cognitive impairment was

found to be 40% by Cummings.  Dementia and cognitive impairment have previously
been reported in the Nigerian PD population.

Osuntokun and Bademosi reported a 5% frequency of dementia in their study of 217

Parkinsonism cases in Ibadan, while Akinyemi et al. in their study of 51 PD cases
reported the frequency of cognitive impairment as 21.6%.
Depression is said to be the most common neuropsychiatric abnormality in PD. The
prevalence worldwide has been documented as varying between 2.7% and
90%,  though the average frequency in most surveys is 40-50%. Variations occur
mainly as a result of differences in methodology. There are no data on frequency of
depression in PD in our environment.

The biochemical basis for cognitive impairment in PD is considered to be low levels of

catecholamine transferase in the mesofrontal cortex resulting from Lewy body
deposition in the cortex. Also, there is reduction in the number of cholinergic
neurons in the nucleus basalis of Meynert.  On the other hand, the biochemical basis
for depression in PD is thought to be predominantly due to a disruption in the
dopaminergic system - dopaminergic denervation of the mesolimbic system and
reduced dopamine transporter activity in the ventral striatum.  Other suppositions
regarding depression in PD are reduction in the noradrenergic neurons in the nucleus
coeruleus and loss of serotonergic neurons in the nucleus raphe.

Loss of serotonergic neurons has been postulated as the common biochemical basis
for both depression and cognitive impairment.

This preliminary study was prompted by the paucity of data in this environment
regarding cognitive impairment and depression in PD and it aimed to determine the
frequency of both NMS in a clinic cohort of Nigerians with PD and to determine the
relationship of either condition alone or in coexistence to PD disease severity and
disability.

2.3.0 Current management of Parkinson's disease

Parkinson's disease (PD) is a neurodegenerative disorder associated with loss of
dopamine-producing neurons in the substantia nigra pars compacta.  James
Parkinson first described the disease in 1817,  and his description remains remarkably
accurate. It is characterized clinically by rest tremor, cogwheel rigidity (stiffness),
bradykinesia (slowness) and postural instability (impaired balance); and
pathologically by neuronal loss and Lewy body formation in the substantia nigra.
Furthermore, similar changes are seen in the peripheral postganglionic sympathetic
nerve fibers, olfactory bulb, the dorsal motor nucleus of the vagal nerve, raphe
nucleus, locus coeruleus, pedunculopontine nucleus, nucleus basalis of Meynert,
amygdaloid nucleus and cortical neurons.  Neurodegeneration of these nuclei is
responsible for nonmotor symptoms and an L-dopa-resistant symptom of PD.   PD
occurs worldwide, but little is known about the epidemiol ogy and genetic studies of
the disease in Africa.  The prevalence of PD in Africa suggests some intracontinental
geographical variation, and overall the prevalence figures and incidence rates of PD
in Africa appear lower than those reported for European and North American
populations. 

Early treatment for PD was disappointing and consisted of anticholinergic

medications to reduce tremor.  The 20 th century witnessed unheralded advancements
in medical and surgical treatments for PD, foremost of which was the discovery that
the dopamine precursor, levodopa, substantially improves motor symptoms.   Today
there are many options for the treatment of PD. This article will focus on drug
therapy in PD.

2.3.1 When to Commence Therapy

The initial question in the management of idiopathic PD is whether any

pharmacotherapy is indicated. To decide upon the timing when to start drug
treatment in PD, particularly in the very early stages of the illness, when there may
be little functional deficit, can be difficult. There is no conclusive evidence that
treatment is helpful before symptoms start to affect the patient's life, although some
neurologists believe that deprenyl, also known as selegiline, could be helpful.  Usually
drug therapy is started when the disability of the patient reaches a certain level
because the currently available anti-Parkinson drugs are considered to have only
symptom-alleviating effects. Once functional deficits begin to interfere with the
patient's work or social activities, treating symptoms becomes appropriate. Initiating
treatment in a patient with PD requires consideration of age, degree of disease
activity and consequences of long-term treatment.

2.3.2 Therapeutic options

There are multiple possible initial pharmacologic choices for the initial treatment of
PD, including monoamine oxidase type B inhibitors, dopamine agonists and
levodopa/ carbidopa.  However, no treatment has yet been proven to affect disease
progression, and the development of medications that can slow the disease process
and thereby forestall disability remains a critical research goal. The pharmacologic
options for patients with early disease include several agents known or presumed to
improve the striatum's surviving dopaminergic activity.
One of these is selegiline. This drug inhibits monoamine oxidase B (MAO-B), a brain
enzyme that would otherwise metabolize dopamine. Inhibition of MAO-B reduces
formation of hydrogen peroxide, presumably reducing intraneuronal oxidative stress.
Based on this, a neuroprotective effect has been hypothesized.
Another option is amantadine, an antiviral medication that provides mild benefit in
treating PD signs and symptoms.  While amantadine's mechanism of action is not
completely understood, it is thought to cause release of dopamine, delay its neuronal
uptake and antagonize another neurotransmitter, glutamine.  It should be used
cautiously in elderly patients and in those with dementia, as it can cause or worsen
hallucinations. Edema of the legs has been troublesome in some patients. However,
it is effective in combination with L-dopa and may reduce the dyskinesias and motor
fluctuations associated with advanced disease. 
Anticholinergic agents are in fact the oldest class of drugs used in PD and are still
given occasionally, either in conjunction with L-dopa or to patients who cannot
tolerate the latter drug. Several synthetic preparations are available, the most widely
used being trihexyphenidyl (Artane) and benztropine mesylate (Cogentin).  As a group,
they are effective in reducing tremor in some patients but have little effect on
bradykinesia and rigidity. In order to obtain maximum benefit from the use of these
drugs, they should be given in gradually increasing dosage to the point where toxic
effects appear: dryness of the mouth (which can be beneficial when drooling of saliva
is a problem), blurring of vision from pupillary mydriasis, constipation and sometimes
urinary retention. These drugs must be used with caution in older adults and in
patients with glaucoma.

Because of the marked dopamine depletion in the brains of individuals with PD

symptomatic treatments have revolved largely around correcting this deficit. Three
main approaches are effective to varying degrees in this regard: using the 1)
dopamine precursor levodopa (L-dopa), 2) drugs that directly stimulate dopamine
receptors bypassing the presynaptic dopamine neurons and 3) drugs that block the
metabolism of dopamine.  Of these, L-dopa continues to be the most efficacious and
is considered the 'gold standard' treatment, which almost all patients with PD require
at some point in the course of their disease and generally for life thereafter. L-dopa is
routinely combined with a peripheral dopa decarboxylase inhibitor, such as
benserazide or carbidopa, which minimizes the gastrointestinal and cardiovascular
side effects of dopamine.  The co-administration of the dopa decarboxylase inhibitor
modestly increases the plasma half-life of L-dopa and doubles its bioavailability,
allowing more of the amino acid to access the brain and exert its intended
therapeutic action.  Several dopamine agonists have been developed, including
apomorphine, piribedil, bromocriptine, lisuride, pergolide, pramipexole, ropinirole
and cabergoline. A common feature is that their efficacy is inferior to L-dopa, with
the exception of apomorphine, which has its own limitations related to
administration route and adverse effects.  The third approach of inhibiting dopamine
metabolism is by blocking catechol-O-methyl transferase (COMT) with entacapone or
tolcapone or by blocking monoamine oxidase B (MAO-B) with selegiline or rasagiline.
These enzyme inhibitors enhance and prolong the effects of co-administered L-dopa.
In addition, MAO-B inhibitors as monotherapy have some anti-parkinsonian efficacy.  

2.3.4 Do we have Neuroprotective Drugs for Parkinson's Disease?

Several drugs were tested for disease-modifying effects in PD, and many others are
being tested in animal experiments and in clinical trials. How far have we gone? We
will review the results on dopamine agonists, L-dopa, MAO-B inhibitors, coenzyme
Q 10 (CoQ 10 ), creatine and minocycline.

2.3.5 Dopamine agonists

Following a period of stable response to dopaminergic medication, PD patients

gradually develop two progressive clinical phenomena requiring changes in the
clinical management: motor fluctuations and dyskinesia.  Studies have shown that
dyskinesias clearly have an adverse impact on the patient's quality of life.  The motor
complications that occur with levodopa administration prompted the development of
alternative medications, including the dopamine agonists (DAs). A change of
handwriting with micrographia is often an early feature of PD as is reduced facial
expression. A loss of arm swing on one side is also an early and useful diagnostic
criterion.  A reduced sense of smell is however worth asking about since this may be
one of the first symptoms in early PD.  DAs are effective as monotherapy in early PD
to improve motor symptoms and as adjuncts to levodopa in patients with motor
fluctuations to reduce off time. The off time also a common and troublesome effect
of chronic use of L-dopa, refers to an unpredictable change in the patient, with
periods of return of PD symptoms when medication effect wears off.  Multiple clinical
trials have demonstrated that initial treatment with a DA to which levodopa can be
added causes fewer motor fluctuations and dyskinesia than treatment with levodopa
alone.  This benefit may be due primarily to delay in the need for
levodopa.  Dopamine transporter single-photon-emission computerized tomography
(SPECT) and fluorodopa photon emission tomography (PET), respectively, tested
pramipexole (Mirapex), a nonergot D2/D3 synthetic aminobenzothiazide derivative;
and ropinirole (Requip), a nonergot DA with strong affinity for D2 receptors. A study
of 301 patients in early stages of PD, followed in a double-blind fashion for a mean of
2 years, after randomization to pramipexole or levodopa (CALM-PD), found marked
reduction in the risk of motor complications in the pramipexole group.   Furthermore,
striatal uptake shows that the rate of loss of dopamine transporters, as measured by
sequential ( 123 I) beta-CIT (2-beta-carbomethoxy-3-beta-(4-iodophenyl) tropane)
SPECT, declined by 16% in the pramipexole-treated patients compared with 25.5% in
L-dopa-treated patients at 46 months from baseline (P = 0.01). 
The use of ropinirole controlled the symptoms of PD satisfactorily, and in addition
reduced the incidence of dyskinesia, compared to treatment with levodopa. A 5-year
study that randomized 268 patients with early PD to either ropinirole (n= 179) or
levodopa (n= 89) to which levodopa could be added when necessary found only 20%
of patients assigned to ropinirole developed dyskinesia, compared with 46% of those
assigned to levodopa.  Putaminal fluorodopa uptake, measured by PET, declined by
13% in the ropinirole-treated patients, compared with 20% in the L-dopa-treated
patients (P = 0.022). The authors concluded that ropinirole as initial therapy slowed
nigral degeneration by 30% compared with L-dopa. Another study found that the
addition of pramipexole to levodopa in patients with motor fluctuations reduced off
time by 17% compared with placebo.

These results can be interpreted as slowing neurodegeneration of nigral neurons in

the dopamine agonist-treated patients.  However, other interpretations are also
possible. First, higher dopamine content in the dopamine uptake sites in L-dopa-
treated patients compared with the agonist-treated groups might have had a
pharmacodynamic effect in terms of decreasing the number of dopamine uptake
sites. The second possibility is that neurons with decreased dopamine uptake sites
are still living cells not reflecting neuronal death. Therefore, the evidence does not
seem sufficient to conclude that dopamine agonists are neuroprotective. 

The usual maximum dose of pramipexole is 4.5 mg/d in three divided doses. It is
started at a dosage of 0.125 mg tds for a week and then titrated to 0.5 mg tds.
Recent reports indicate that pathological gambling may be associated with DAs,
especially pramipexole, usually at higher doses. In one review, the incidence of
pathological gambling was 1.5% in patients taking pramipexole (mean dosage, 4.3
mg/d; range, 2 to 8 mg/d), compared with an overall incidence of 0.05% in patients
with PD regardless of therapy.  Excessive shopping and hypersexuality are other
forms of impulse-control disorders that may occur with DA use. Patients should be
warned about these behaviors when DAs are prescribed, and DA dosages need to be
reduced if these problems emerge. The recommended initial dosage for ropinirole is
0.25 mg three times daily (total 0.75 mg/d). Pergolide (Permax), an ergot with strong
affinity for D2 receptors, is effective in reducing motor symptoms in PD. Several
studies have shown that the use of pergolide permits a significant reduction in
levodopa dosage when it is used as adjunct therapy in patients with motor
fluctuations compared with placebo.  Pergolide is usually initiated at a dose of 0.05
mg for the first two days and increased by 0.1 mg/d or 0.15 mg/d everyday over the
next 12 days. Studies have identified an increased frequency of valvular heart disease
in patients taking pergolide. This appears to be a potential side effect of all ergot
agonists, and the mechanism is believed to be activation of 5-hydroxytrptamine 2B
(5-HT 2B ) receptors. 

2.3.6 Levodopa

Levodopa remains the most effective medication to improve motor features of PD

with the fewest short-term side effects. It effectively ameliorates bradykinesia and
rigidity but is variably effective for tremor.  By combining a decarboxylase inhibitor
(carbidopa or benserazide), which is unable to penetrate the central nervous system,
with levodopa, the decarboxylation of levodopa to dopamine is greatly diminished in
peripheral tissue. This permits a greater proportion of levodopa to reach nigral
neurons and at the same time, a reduction in the peripheral side effects of levodopa
and dopamine (nausea, hypotension etc). The Parkinson Study Group   compared the
effect of L-dopa versus placebo on disease progression. Early-stage PD patients were
divided into 4 groups: those who received L-dopa/carbidopa 150, 300 or 600 mg/d
and placebo groups. Patients were treated for 40 weeks and medication was
discontinued for 2 weeks. Outcome measures were Unified Parkinson Disease Rating
Scale (UPDRS) score and the beta-CIT SPECT. The UPDRS has long been the major
rating scale that is used to assess severity of symptoms of PD. The original version of
the scale assessed daily activities, motor skills and mental capacity (including
behavior and mood). The higher the UPDRS score, the greater is the disability due to
PD. All of the L-dopa groups showed significant improvement of the UPDRS scores
compared with the placebo group. After the 2-week drug washout period, UPDRS
scores in all L-dopa groups returned to near-baseline levels; on the other hand,
UPDRS scores were significantly worse than baseline levels in the placebo group.
UPDRS score after drug washout was best in the L-dopa 600 mg group. These results
suggest that L-dopa has a disease-modifying effect in PD; the disease-modifying
effect may be due to neuroprotection of the substantia nigra or neuroplasticity effect
on neuronal networks. Whatever the mechanism, early use of L-dopa appears to be
good for PD patients, as evaluated by UPDRS. On the other hand, however, beta-CIT
showed opposing results: a decline in the decrease of beta-CIT uptake was largest in
the group treated with L-dopa 600 mg. Guttman et al. Reported reduced uptake of
beta-CIT in early-stage PD patients treated with L-dopa. However, other studies
showed no effect of L-dopa treatment on striatal beta-CIT uptake and fluorodopa PET
scan.  Another possibility entertained was that low dopamine in the placebo group
up-regulated dopamine transporter activity, resulting in a smaller decline in beta-CIT
uptake. The answer to the question as to whether L-dopa has disease-modifying
effects must await further studies.
2.3.7 Entacapone

The idea of using catechol-O-methyltransferase (COMT) inhibitor was proposed in

the 1950s, but no effective and safe substances were available at that time.   The idea
to use COMT inhibition re-emerged in the early 1980s. Double-blind, placebo-
controlled trials have demonstrated that entacapone increases "on" time, decreases
"off" time and improves motor scores for patients with PD who experience motor
fluctuation.  Entacapone (Comtan) is a selective, reversible peripherally acting COMT
inhibitor that is used in conjunction with carbidopa/ levodopa to extend the levodopa
half-life and allow more levodopa to be delivered to the brain over a longer time. The
addition of entacapone reduced "off" time in patients with motor fluctuations on
controlled release carbidopa/levodopa.  Stalevo is a combination of carbidopa,
levodopa and entacapone and is available as Stalevo 50, 100 and 150.

  2.3.8 Monoamine Oxidase Type B Inhibitors

The deprenyl and tocopherol antioxidative therapy of Parkinsonism (DATATOP) study

initially suggested disease-modifying effects of selegiline.  However, further analysis
revealed that this was accounted for by the symptomatic effect of
selegiline.  Palhagen et al. looked at the question of the disease-modifying effects of
long-term selegiline administration versus placebo therapy in early-stage de novo PD
patients. Patients initially assigned to selegiline showed less progression as evaluated
by total UPDRS score at 4 years and tended to delay wearing off compared with
placebo (34% versus 20%), but there was no difference between the two groups in
the time taken to develop dyskinesia. Thus, these researchers postulated that
selegiline might have a delaying effect on the progression of PD. The study conducted
by Olanow et al. also suggested a disease-modifying effect of selegiline. Rasagiline
(Azilect) is a new irreversible MAO-B inhibitor with anti-apoptotic and antioxidative
properties. Its effect on disease progression in PD was tested in a unique way. The
Parkinson Study Group  investigated rasagiline in early-stage drug-naοve PD patients
in a delayed-start study design. Patients were allotted to three groups receiving
rasagiline 1 or 2 mg/d or placebo, respectively. After 6 months, patients in the three
groups were re-randomized to receive rasagiline at either 1 or 2 mg/d; thus after 6
months, all patients enrolled received rasagiline. It was hypothesized that if the
effects of rasagiline were purely symptomatic, then the placebo group that received
rasagiline afterwards would catch up with the initially assigned rasagiline groups. As a
result, the UPDRS scores of the initial placebo and initial rasagiline groups became
parallel. This was interpreted as indicative of the disease-modifying effect of
rasagiline.
 2.3.9Coenzyme Q 10

Coenzyme Q 10 is a cofactor for complex I, which acts as a bioenergetic and an

antioxidant. It has been tested as a putative neuroprotective agent in PD based on
laboratory studies showing that it protects dopamine neurons in PD models.   Shults et
al. studied the effects of high-dose CoQ 10 on the development of disability in early PD
patients. They randomized 80 patients who were not yet on L-dopa to receive
placebo or one of the three doses of CoQ 10 , viz., 300, 600 or 1200 mg/d, for a follow-
up period of <16 months. The primary response variable was change in total UPDRS
score. Subjects treated with CoQ 10 had less disability as shown by a change in UPDRS
from baseline (8 in controls and 6.4 in the 1,200-mg group) (P = 09). Although the
results did not reach statistical significance, they did meet pre-specified criteria for
positive trends. However, the authors concluded that their results need confirmation
in large phase III studies and that until then it would be premature to recommend the
use of CoQ 10 for the treatment of PD.

2.3.10 Creatine

Creatine is widely used as a health food; as a component of creatine phosphate, it

forms part of the most important energy reservoir for adenosine triphosphate (ATP).
Studies have suggested that it can improve the function of mitochondria, which
produce energy inside cells. It also may act as an antioxidant that prevents damage
from compounds that are harmful to cells in the brain. The National Institute of
Neurological Disorders and Stroke Neuroprotection Exploratory Trials in Parkinson
Disease (NINDS NET-PD) investigators treated a cohort of de novo PD patients with
either placebo or creatine. Mean decline of total UPDRS score at the end of 12
months was 5.6 in the creatine group and 8.39 in the placebo group; the difference
was small but statistically significant. The authors concluded that creatine warrants
further study in randomized controlled trials (RCTs) to assess whether it has disease-
modifying effects in PD.

Minocycline, a tetracycline derivative, is a caspase inhibitor, and it inhibits the

inducible nitric oxide synthases, which are important for apoptotic cell death.
Furthermore, minocycline has been shown to block microglial activation of 6-
hydroxydopamine and 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine-lesioned
Parkinsonism in animal models and protect against nigrostriatal dopaminergic
neurodegeneration.  Because inflammatory processes might be involved in the
progression of PD, anti-inflammatory agents could have neuroprotective effects. The
NINDS NET-PD investigators  studied minocycline in the same way as they assessed
creatine and noted that the average decline of UPDRS score at the end of 12 months
was 7.09 in the minocycline group and 8.39 in those assigned to placebo. These
studies were done as part of a futility study that was introduced to screen drugs that
might have disease-modifying effects in PD.

In summary, our review of the literature on pramipexole, ropinirole, levodopa,

selegiline, rasagiline, CoQ 10 , creatine and minocycline suggests that these agents
might elicit small disease-modifying effects in PD. It is not known whether this is due
to slowing down of the neurodegenerative processes, effect on the plasticity of the
brain, a combination of both or due to some other mechanism. So far, none of the
tested drugs for PD has explicitly been shown to have neuroprotective effects.

2.3.11   Conclusion: Where Do We Stand in the Treatment of PD?

PD is age-related neurodegenerative disorder with an average age of onset of about

60 years, and it occurs worldwide but appears to be less common in Africa than
elsewhere in the world. With the ageing of the population, the frequency of PD is
expected to increase, perhaps slowly in the developing countries, because of the high
prevalence of chronic diseases such as malaria and HIV/ AIDS. A goal of vital
importance in neuroscience today is to elucidate the etiology of neurodegenerative
disorders - a prerequisite for the development of curative therapy. Although our
insight into the great complexity of pathophysiological mechanisms in PD has rapidly
increased, introduction of effective neuroprotective or curative clinical treatment in
this disease is not expected in the near future. On the other hand, regarding
symptomatic therapy the situation is quite different. Today we have many options for
the treatment of PD. Symptomatic treatment should be considered for patients with
functional impairments caused by PD. The therapeutic goal is to reverse functional
disability, completely if possible, without leading to short- or long-term side effects
and toxicity. Although L-dopa is still the gold standard of treatment, relying solely on
levodopa may cause various problems in the long term.
Abrevation
PD:
Parkinson's disease
2.4 Clinical profile of parkinsonism and Parkinson's disease in Lagos,
Southwestern Nigeria
This study provides a description of the current clinical profile of PD and secondary
parkinsonism as seen over the last ten years at a tertiary referral centre in South-
western Nigeria. The spectrum of cases encountered may thus be subject to referral
bias, with a tendency to see more severe or more complex neurological cases. The
study however provides data for comparison with an earlier report and global
perspectives of parkinsonism and PD.

In contrast to the only published report on the clinical characteristics of parkinsonism

in Nigerians from Osuntokun and Bademosi, PD accounted for a significantly higher
proportion of causes of parkinsonism in the present study (79% compared to 38%).
The current relative frequency of PD in our study is in keeping with available
literature, which ranks PD as causing approximately three quarters of all cases of
parkinsonism. The apparent disparity may be accounted for by more recent
improvements and streamlining of the diagnostic criteria for PD and other
parkinsonian syndromes in both the clinical and research arena in contrast to the
status at the time of the earlier report.

The clinical profile of our patients differed slightly from that reported in the earlier
Nigerian study. First, the mean age at onset in the present study was 61.5 years,
higher than the 55.6 years reported by Osuntokun et al. Both studies represent
patients seen in the same geographical region, with both tertiary centres being
within two hours' drive of each other. The increase in age at onset may thus be an
accurate phenomenon akin to that observed by Hoehn and Yahr in which they found
a time trend of increasing age at onset over decades of study. It has been
documented that as populations age, the age at onset of PD tends to increase. The
male preponderance reported in the earlier study (ratio 4.5 to 1) was also
documented here, but the magnitude in this study was lower (ratio 3.3 to 1).
Although this male predilection appears to be a consistent finding, the precise reason
is unknown, and the possibility of a neuroprotective effect mediated by estrogen in
women exists [15–17]. Experimental evidence indicates that estrogen may mediate
this effect via several mechanisms including inhibition of dopamine transporter
affinity and prevention of entry of neurotoxic agents into dopaminergic nerve
terminals, thereby reducing nigrostriatal degeneration.

Genetic contributions to the aetiology of PD are undisputable, with transmission as

an autosomal recessive or dominant trait linked to mutations in several genes,
including α-synuclein, parkin, DJ1, leucine-rich repeat kinase (LRRK) 2, etc. Genetic
susceptibility appears to be more apparent (although not exclusive) in young onset
PD compared to persons developing the disease after the 6th decade of life. We found
a positive family history of PD in a first degree relative in only one of our patients
who incidentally had young onset PD starting below age 50. Young onset PD was
documented in 16.3% of our cohort, with a five-fold higher frequency in men (20%)
compared to women (4.3%). We acknowledge the fact that the number of PD cases
reported here (including only 23 females) is small and may account for the low rates
of a positive family history and gender disparity in frequency of young-onset PD; our
findings are thus subject to further validation. A preliminary analysis of the genetic
contributions to PD in Nigerians (which included some of the cases reported in this
present study), explored the role of mutations in LRRK2, PRKN and ATXN3 in
apparently sporadic PD compared to age - and ethnically-matched controls. The
study found that common pathogenic mutations in these genes, previously observed
in several populations, are not a frequent cause of PD in Nigerians.

Overall, the clinical profile of PD in Nigerians does not appear to vary substantially
from disease characteristics reported in other populations. Delayed presentation
(and late referral) are not germaine to this study population and is one of the
challenges encountered in managing PD in Africa. Poor recognition of the cardinal
features of parkinsonism and of the existence or benefit of available therapies in
alleviating the symptoms and improving the quality of life of people with PD may
contribute to late referrals. This has further implications as it will delay utilization of
disease-modifying strategies which may become available in the future. Strategies to
improve early recognition and referral include strengthening undergraduate
movement disorders curriculum, and improving public awareness as to the existence,
cardinal features, and treatment options of parkinsonism via the media. The need for
such an approach is strengthened by the increased likelihood of physicians
encountering PD and other neurodegenerative diseases of the elderly in the future in
developing countries experiencing an epidemiologic transition marked by aging of
the population.

We acknowledge the methodological limitations of this study in that follow-up data

on the disease course and rate of progression, and an objective measure of
magnitude of response to levodopa therapy, and mortality data which would
enhance insight into the phenotypy of our PD cohort are lacking. An earlier published
study of a subgroup of this cohort (28 PD cases and 28 age-matched controls) initially
seen between January and June 1997 and followed up between January and May
2003 (after a 6-year interval) reported a case fatality rate of 25% in PD, compared to
7.1% in controls. The peculiarity of our clinical practice scenario, characterized by the
availability of a very narrow spectrum of antiparkinsonian medications and dosage
formulations is reflected in the distribution of medications used in PD treatment in
our cohort. We also emphasize that this factor would also limit the conclusiveness of
any description of treatment outcomes in our cohort at the present time.

ADL:
Activities of Daily Living
H&Y:
Hoehn and Yahr
PD:
Parkinson's disease
UPDRS:
Unified Parkinson's Disease Rating Scale
WHO:
World Health Organization
SD:
Standard deviation.

2.5 Epidemiology of Parkinsonism and Parkinson's disease in Sub-Saharan Africa:

Nigerian profile
Parkinsonism and Parkinson's disease (PD) are the most common movement
disorders (neurological syndromes characterized by paucity of voluntary and
automatic movements or excessive movements unrelated to muscle weakness or
spasticity), and they are generally perceived to have lower prevalence and incidence
in Sub-Saharan Africa (SSA) because of the relative youthfulness of the SSA
population (<5% are over 65 years of age), under-recognition, paucity of published
reports, and cultural perception of neurologic disorders generally as being part of
normal ageing.[1]
In Nigeria, Africa's most populous nation, the earliest detailed report on
Parkinsonism and PD dates back to about 40 years ago when Osuntokun[2] described
extra pyramidal disorders in 1.9% of 9600 patients with neurological conditions seen
over a 12 year period (1957–69) at the University College Hospital Ibadan,
Southwestern Nigeria. Most subsequent reports on this syndrome from Nigeria have
emanated similarly from the same region, the current report by Owolabi et al[3]
being the very first from the expansive northern region of the country.
In 1978, Osuntokun and Bademosi described 217 Nigerians with Parkinsonism, of
whom 38% were classified as PD. However, in a recent 10 year review of
Parkinsonism as seen in the major tertiary hospital in Lagos, the Nigerian commercial
nerve center in the Southwest, 79% of the 124 patients reviewed had PD[4] a figure
very close to the 83% documented from the current review from Kano, Northern
Nigeria. The increased proportion of PD is thought to be due to recent refinements in
the diagnostic criteria for PD and Parkinsonism syndromes. The spectrum of
secondary Parkinsonism and Parkinson-plus syndromes documented from these
hospital series and other anecdotal reports in Nigeria includes Parkinsonism
secondary to Wilson's disease, cerebral vascular disease, drugs, trauma, tumor
excision, typhoid septicemia, and human immunodeficiency virus (HIV) infection.
Others are multiple system atrophy, dementia with Lewy bodies, progressive
supranuclear palsy, hemi-parkinsonism-hemiatrophy, juvenile parkinsonism with
dystonia and hemiatrophy and primary amyloidosis with parkinsonism.
A pioneering epidemiologic survey of PD from a rural community in Southwestern
Nigeria yielded an age-adjusted prevalence rate of 67 per 100,000 (above 39 years),
[5] while a case-control study on risk factors found blacksmithing (OR 8.0 95% CI 1.3-
50.7) to be significantly associated with PD. There are no data on exposure to
pesticides, herbicides, rural living, and well water use. A preliminary analysis of the
genetic contributions to PD in Nigerians explored the role of mutations in LRRK2,
PRKN, and ATXN3 genes and found some novel but non-pathogenic mutations.
Neuropathological studies involving brain tissue samples of neurologically normal
Nigerians showed number of melanized neurons and Lewy body pathology burden[9]
similar to findings in Caucasian populations implying that the frequency of PD-related
pre-symptomatic neuropathology (and indirectly the risk of PD) among Nigerian and
Caucasian populations may be similar, but the effect of yet unidentified genetic
factors, environmental exposures, differences in population structure and reduced
life expectancy of Nigerians (about 50 years) may explain the differences in the
prevalence and incidence rates observed between the two population groups.
Findings from this seminal work of Owolabi et al reveal some shared features of PD in
both Northern and Southern Nigeria.These include onset of disease in the sixth
decade, male preponderance, under-diagnosis, late presentation, higher mortality,
higher proportion of tremor dominant PD, and relatively low proportion of young
onset and familial disease compared to Western populations. However, the relatively
older age of onset in the current study compared to older studies may be a subtle
evidence of ongoing epidemiologic transition.
Non-motor manifestations including cognitive dysfunction, autonomic dysfunction,
psychiatric symptoms (especially apathy, depression, and anxiety), gastrointestinal
and sudomotor disturbances all of which significantly impact patients’ quality of life
have also been described among Nigerian PD patients.
The management of PD in Nigeria is fraught with challenges which include high cost
and narrow spectrum of available treatment options and medications, paucity of
movement disorders specialists, late presentation occasioned by poor public
awareness and wrong cultural perceptions of the disease and high caregiver burden.
Overall, though the current report represents an important milestone in the annals of
movement disorders in Nigeria and SSA, there still exist knowledge gaps in several
aspects including current prevalence and incidence, natural history, quality of life,
cost of care, treatment outcomes and clinico-genetic-pathological correlations of PD
and other movement disorders. Intra- and international collaborations are needed to
enhance research and capacity building while advocacy through public awareness
campaigns and support groups will improve the recognition and adequate holistic
treatment of Parkinsonism and PD in rural and urban SSA.

2.6 Depression among Patients with Parkinson's Disease in a Nigerian Tertiary

Hospital.
INTRODUCTION Depression is the most common non-motor symptom of PD . It has
been the focus of numerous research studies in PD. Depression in the context of PD
can be reactive, caused by the incurable, progressive nature of the disease, and
therefore can be an understandable reaction to disease and its consequences. On the
other hand, there is a widespread and severe disruption of monoaminergic
neurotransmission, predisposing to depression. Depression in patients with PD
should thus be treated as a single entity. Depression is often overlooked by
physicians because of the many shared clinical features between the two disorders,
such as weight loss, sleep disturbance, fatigue, sexual dysfunction, forgetfulness, and
bradykinesia. If the physician brings up the topic by asking specific depression-related
questions, most patients will be honest and will discuss their mental state, although
they often will not bring up "depression" themselves or identify the changes they are
experiencing as depression [10]. Estimates of the incidence of comorbid depression
vary widely, from 4% to 75%[11]. There are variations in incidence of depression in
PD due to few epidemiological studies. The available surveys in research centres
diagnose depression in 40% to 50% of patients with PD compared to community-
based studies which have rates of depression that are less than 10%[1]. Rates of
depression in PD have also been shown to vary widely between different countries.
Surveys in Norway and China found the rates of major depression were 7.5% and
16.5% respectively. The Global Parkinson's Disease Survey, which included 1000
patients, 200 clinicians, and 187 caregivers in five countries including the US, found
that approximately half of PD patients had depressive symptoms that significantly
impacted their daily functioning. The fact that no Mrican country was included in this
study lends credence to the assertion that the exact frequency and pattern of
depression among Mricans has not been fully studied particularly in Mrica. It is
known that in comparison to the general population, there is a considerable
enhanced risk of depression in Parkinson's disease thus requiring that the physician
screen all PD patients for depression [14].Additionally, depression can impair both
fine motor skills and cognitive function and is a primary factor negatively affecting
HRQOL in PD . Using the Beck Depression Inventory II (BDI11) as a psychometric
measure of depression, this study set out to determine the frequency and severity of
depression among Nigerians with PD presenting at the University of Port Harcourt
Teaching Hospital. It will also relate the frequency and severity of depression to the
stage and severity of PD. We hope that results from this study will serve as a basis for
comparison with studies among PD patients from other population and help fill the
void created by a dearth in literature of studies on depression among Parkinson'
disease patients in settings similar to ours. We however hypothesized that patients
with PD would be depressed compared to the control group and the severity of
depression will be worse in more advanced PD

2.7 A Nationwide Survey of Parkinson's disease Medicines Availability and

Affordability in Nigeria

Parkinson’s disease (PD) is one of the top 10 neurological dis-eases encountered in

primary care in Africa and the sixth-most frequent neurological disease in specialist
care.1The Global Burden of Disease Study 2015 ranks PD 11th globally and in most of
Africa with respect to attributable burden measured using age-standardized disability
rates.2The number of persons with PD in developing countries is projected to
increase from2.37 to 3.08 million between 2015 and 2030.3Data from the United
Nations (UN) indicate that more than half of the global population growth between
2015 and 2030 will be from Africa.4This population growth is attributed to projected
prolonged life expectancy and aging of the population. Nigeria currently has the
seventh-largest population in the world, and is the most rap-idly growing, with its
population expected to surpass that of the United States by 2050, at which time it
would become the thirdlargest in the world.4Given that PD affects approximately 1%
of persons aged 65 to 85 years, and 4.3% of those > 85, considering the projected
population expansion and survival into old age in Nigeria, the burden of PD will
certainly become more immense in the near future.5In spite of the growing numbers
of people with PD globally, access to health care in general, and medications in
particular, remains problematic. The UN Development Group (2003)defines access as
“having medicines continuously available and affordable at public or private health
facilities or medicine outlets that are within one hour’s walk from the homes of the
popula-tion.”6Access is a multidimensional concept that encompasses availability,
acceptability, affordability, and accessibility. The sec-ond edition of the World Health
Organization (WHO) Neurology atlas published in 2017 reported that drugs for PD
were available to only 3% who needed them in primary care in Africa(in contrast to
69% in Europe and 34% global average).7Pilotsurveys suggest that there has been
little or no change in PD medicines availability in most African countries, and wide
intra-and inter country variability is highly probable.8,9The Global PD Charter
emphasizes this challenge, stating that “world governments and all healthcare
providers should take strong and decisive action in making PD a public health priority
area ”and“ ensure people with PD receive appropriate treatment.”10In addition, the
charter advocates for improved access to care across the full spectrum of PD.10The
present survey was aimed at investigating the availability and affordability of PD
medicines in Nigeria, as part of a wider sub-Saharan Africa (SSA) initiative of the
International Parkinson and Movement Disorder Society (MDS) Task Force on Africa
to determine the status of access to PD medicines in Africa. The specific objectives
were to determine the availability and assess the cost and affordability of anti-
parkinsonian medications in pharmacies across Nigeria. Such data are indispensable
as an objective basis to inform policy change and advocate for improved access to
medicines for people living with PD.
.

2.8.0 The challenge of Parkinson's disease management in Africa

It has been suggested that Parkinson's disease (PD) is seen less frequently in
populations of African origin. Worldwide crude prevalence rates have varied from 7
(in Ethiopia) to 405 (in Uruguay) per 100,000 of the population. Whether there is a
true difference in susceptibility of these populations would be of great importance
epidemiologically, in terms of investigating the cause(s) of PD. However, this
difference could be accounted for by several factors: under-diagnosis of PD in these
communities, differences in case finding methods, differences in diagnostic criteria
used and early mortality owing to other causes in these populations.
Previous studies in sub-Saharan Africa (SSA) have been performed using differing
methods, making them difficult to compare with each other and other studies
elsewhere in the world: door-to-door studies carried out by Osuntokun et
al. (Nigeria) [4] and Tekle-Haimanot et al.  (Ethiopia); case finding from neurological
clinics and neurological admissions by Harries et al. (Kenya) and Bower et
al. (Ethiopia) [6]; retrospective review of hospital admissions by Lombard and
Gelfand [1] (Zimbabwe); and using data on levodopa (L-dopa) usage by Cosnett et
al. (South Africa) [7]. Most of the studies have been on small population sizes and
most are now over 20 years old. As there are few studies, papers describing both
idiopathic PD and Parkinsonism are included. Within each section, we have tried to
make it clear exactly who was included in the study. Unless stated, the African
studies are all on the basis of black African populations.
2.8.1 Door-to-door studies in Africa
In 1986, a door-to-door study was performed by Osuntokun et al.  in a Nigerian town,
Igbo-Ora, with a population of 20,000. They looked at all neurological disorders, not
specifically PD. They used a two-step procedure, with a screening questionnaire
carried out by non-medically trained administrators, followed by an expert history
and examination if they answered positively to the questionnaire. Nearly 95% of the
population took part in the study. Only 11% of the population were over 50 years
(compared with over 33% in the United Kingdom). No diagnostic criteria for PD are
described. Their results showed a point prevalence rate for PD of 10 per 100,000, i.e.
only two cases were identified. The age and sex of these cases is not reported.

A second door-to-door survey was carried out by Tekle-Haimanot in rural Ethiopia

between 1986 and 1988. Again, this study, which included a population of 60,820,
looked at all neurological disorders, and not just PD. Participation rates were
between 95 and 100%. The median age of this population was 14.5 years with 59% of
the population being <20 years old. They found four cases of PD (all male), giving a
crude prevalence rate of 7 per 100,000. No diagnostic criteria for PD were
documented. The authors state that the reason for the difference in the prevalence
of PD among white populations is due to the difference in population age structure.
However, age standardised rates were not calculated.

2.8.2 Studies using retrospective review of hospital admissions

Lombard and Gelfand [1] looked at notes from admissions of black Africans to Harare
Hospital between 1973 and 1976 and compared this to admissions to a nearby
hospital covering a white African population (the Andrew Fleming Hospital) in 1974–
76. There were 17 admissions of cases of PD (nine female and eight male) in the black
population over that time period compared with 33 in the white population.
However, the total number of admissions in the former hospital was 82,453 from a
population of 430,000 compared with 34,952 of the total white admissions from a
population of 126,000. To try and correct for the difference in population sizes, they
multiplied the number of cases in the white population by 3, showing a big
discrepancy between the two races (17 in the black population versus 99 in the white
population). Of course, as this is a hospital-based study, cases in the community
would not have been taken into account. No diagnostic criteria for PD are mentioned,
although they do report that none of the cases had a prior history of encephalitis and
carbon monoxide or manganese poisoning was thought to be unlikely. However, one
patient was on a neuroleptic drug (chlorpromazine) and vascular Parkinsonism was
suspected in a few patients. Therefore, it is unlikely that this entire group had
idiopathic PD.

2.8.3 Studies of neurological outpatient consultations

Using retrospective records from the neurological consultations and data on the
usage of L-dopa, Cosnett and Bill [7] reviewed the presentation of black patients in
Natal, South Africa and compared this to local Indian and white African populations.
Over a 7-year period (1979–85 inclusive), 1,984 black patients were reviewed by a
neurologist and only three cases of idiopathic PD were noted (age and sex not
reported). PD diagnosis was based on ‘the grounds of bradykinesia, rigidity, resting
tremor and postural instability’. Ten patients were felt to have a diagnosis of
‘secondary’ Parkinsonism, which the authors classify as being due to drugs, hypoxia,
encephalitis or typhoid fever. Within the black population, 22.8% were over the age
of 50, 9.4% over the age of 60 and 1.8% over the age of 70. In the same population of
white patients attending neurological clinics, 47.8% of the population were over 50
years. The authors also looked at the frequency of L-dopa prescription. In the black
population, there was approximately nine times less L-dopa prescribed than in the
white populations. They propose that one reason so few cases were seen, was an
early selective mortality in the black population. It was suggested that the elderly
blacks were less likely to seek medical attention than other races. However, similar
numbers of black and white patients with motor neurone disease were seen.
A recent paper (2005) reported a review of consultations at a university hospital
neurology clinic in Ethiopia . One hundred and nine patients with movement
disorders were seen at the clinic in 2003–04. This accounted for over 15% of all
referrals. Of the 720 patients 52 had Parkinsonism, of whom 46 were diagnosed with
idiopathic PD. The diagnostic criteria used are not mentioned. There was a male
predominance. Interestingly, and in contrast to other reports, 90% of patients were
treated with L-dopa, but, in contrast to the UK practice, 82% were also taking an
anticholinergic medication. Fourteen of the patients on L-dopa had financial concerns
regarding their medication, compared with only two taking the anticholinergic
medications. The authors comment that they are unaware of the prevalence of PD in
their community, and so do not know how many have not sought, or cannot afford,
help.
2.8.9 Use of L-dopa in Africa
Harries [5] looked at the use of L-dopa for Parkinsonism in African patients in 1972.
All patients were said to have idiopathic PD, although no diagnostic criteria are
documented. He begins his article by saying that PD is not uncommon in Africans,
and indeed he had noticed 30 cases in the previous 5 years in his outpatient clinic in
Nairobi, Kenya. He chronicles the use of L-dopa in seven patients (six male and one
female) aged 43–65 years. It is not clarified whether these are black or white
Africans; however, they were reported to converse in Kiswahili, making it seem likely
that they were black African patients. All except one patient made an improvement
as defined by the Webster rating scale and all patients reported increased well being
on the treatment. Side effects were noted in five of seven cases: constipation,
hallucinations (thought to have been related to benzhexol introduction and not the L-
dopa alone), dyspepsia and dystonia.
2.8.10 Clinical presentation
Haimanot [8] looked prospectively at 70 cases of PD in Ethiopia who attended his
private neurology outpatient clinic at a teaching hospital between 1980 and 1984.
Diagnosis was based upon the presence of bradykinesia, rigidity and tremor,
although it is conceded that patients with Parkinsonism owing to other causes (e.g.
vascular disease) may have been included. Additional factors that helped strengthen
the diagnosis were facial masking, abnormal postural reflexes, typical gait
disturbance, speech disturbance and autonomic dysfunction. Data on age at onset of
disease, current age, sex, initial symptoms of PD, history of head injury, use of
neuroleptic drugs, syphilis infection and previous encephalitis were recorded. He also
checked various blood tests and skull X-rays were requested in 63 patients. During
this period of the study, only two patients were actually admitted to hospital, and the
others were managed on an outpatient basis. This confirms that using the number of
hospital admissions to estimate the impact of PD misses the majority of cases. During
the same period of study, four patients died of pneumonia and one from a
malignancy. PD was seen more frequently in males (7:3) and the commonest decade
was 61–70 (25 cases). Four of the cases identified were under 40 years. The mean
age at onset of symptoms was 54.6 years. The most common presenting symptom
was tremor (90%) followed by bradykinesia (86%) and stiffness (71%). In 70% of
patients their symptoms had been unilateral at onset, but progressed to involve the
opposite side. Twenty-one patients had previously suffered a significant head injury
(one of whom had a depressed skull fracture on X-ray), six patients had a positive
venereal disease research laboratory test (but only one had features suggestive of
neurosyphilis) and, interestingly, one patient gave a family history of PD (his father
had died at the age of 68 and never received any treatment for his symptoms). Most
patients did not present themselves to a doctor until they had had symptoms for 2–5
years and at presentation, only 22.9% had Hoehn and Yahr stage I (early) disease, and
10% had stage V (late) disease. Again, lack of continuous availability of medication
was a problem and most were treated with benzhexol, with only a few receiving L-
dopa. Haimanot concludes that black races are relatively protected against PD.

Lombard and Gelfland also discuss the presentation of PD in their cases. They
reported tremor as being the main feature in nine patients, and tremor and rigidity in
two patients. Only one case is reported as having bradykinesia, a prerequisite for the
diagnosis of PD in the UK PD brain bank criteria.

2.8.11 Perception of PD in Africa

Perception of PD in Africa is likely to be different from other areas. Often, patients

with neurological disease such as epilepsy or leprosy are seen as ‘cursed’ and as a
result are often cast out of society [8]. The cultural norm tends to be to visit
traditional healers before seeking medical help and as a result patients tend to
present later than those in developed countries, if at all. Haimanot also noted that
several Parkinsonian patients had ended up as beggars, as their visual appearance
aroused sympathy in the public. This may well have an impact on whether the
patients present to western medical care or to a traditional healer. It may also mean
that patients with these symptoms would try to conceal them. Both these factors will
have an impact on how frequently PD is seen in hospitals and by medical
practitioners, meaning they are important considerations in any report on the
prevalence of PD in Africa.

2.8.12 Autonomic symptoms in African patients with PD

Autonomic dysfunction is well recognised in PD, particularly as the disease
progresses. Okubadejo et al. [9] studied the frequency of autonomic dysfunction in
33 patients with PD in Nigeria and age-matched controls. Autonomic function tests
utilised included heart rate variability to deep breathing, standing and the Valsalva
manoeuvre and blood pressure response to standing. The found that autonomic
dysfunction was common in Africans with PD, especially those over the age of 65.
Among the patients with PD, 51.5% had abnormal parasympathetic function, which
was significantly higher than controls, although many of these patients (41.2%) had
no symptoms associated with it.
2.8.13 Services available in Africa to support patients with PD

The WHO Neurology Atlas [10] compares neurology services by continent, based on a
questionnaire sent out to 106 member states including 16 countries in the African
region. The African responders reported 0.03 inpatient neurology beds per 10,000 of
the population. On average, there were only 0.03 consultant neurologists per
100,000 of the population, and all African populations reported <1 consultant
neurologist per 100,000 of the population. Drugs for PD in Africa were available to
only 12.5% of those who needed them, compared to 79.1% in Europe. As nearly 60%
of the population live off less than $2 US per day , it is unlikely that they will ever be
able to afford treatment, be it pharmaceutical, expert medical or informal help with
care.

2.9 DISCUSSION
This review has highlighted several important issues concerning Parkinson’s disease
in Nigeria. First, the potential role of herbs in the treatment of Parkinson’s disease, its
pathophyiology, the pathogenesis of Parkinson’s disease, the apoptosis and its
oxidative stress involvement of Parkinson’s disease
Secondly, an evaluation of neuropsychiatric symptoms in Parkinson’s disease
patients.
Thirdly the frequency of cognitive impairment and depression in Parkinson’s disease:
A parliaminary case-control study.

A further view on the current management for Parkinson’s disease and more insight
on when it commence therapy, its therapeutic options, even went further as explain
many asked questions on neuroprtective drugs for Parkinson’s disease, a long review
on dopamine agonists, levodopa review as well, entacapone review, monoamine
oxidase type b inhibitors, coenzyme Q10 roles, creatine review and a conclusion of
where we stand in the treatment of Parkinson’s disease using this methods.

Furthermore, a deep in sight on clinical profile of parkinsonism and Parkinson’s

disease in Lagos, southwest Nigeria also another topic that focused on the
epidemiology of parkinsonism and Parkinson’s disease in Sub-Saharan Africa:
Nigeria.

A deep insight of depression among patients with Parkinson’s disease in Nigeria

Tertiary Hospitals was reviewed in this literature.

Also a review on the nationwide survey of Parkinson’s disease medicine availability

and affordability in Nigeria.
Lastly a review of the challenge of Parkinson's disease management in Africa which
consisted of sub topics like Door-to-door studies in Africa, Studies using retrospective
review of hospital admissions, Use of L-dopa in Africa, Clinical presentation,
Perception of PD in Africa, Autonomic symptoms in African patients with PD, Services
available in Africa to support patients with PD and finally a discussion to wrap it up

In addition to the above observation is the fact that most of the studies carried out in
the various geopolitical zones, were mainly retrospective, and analysed health facility
data of Parkinson’s disease tertiary level. This underscores the concept and fact that
Parkinson’s disease activities are basically primary care. There have been very few
programmatic and social science studies done in the rural communities where
majority of the population resides.

Furthermore, it is significant to note that most of the studies were knowledge,

attitude, and practice studies. There is a paucity of program evaluation and
intervention studies that assess service delivery in terms of distribution, availability,
and accessibility of Parkinson’s disease herbal treatment.

There are also very few communication, health education, and information
technology studies that assess the role of these herbal medicinal treatment for
Parkinson’s disease in healthcare structures. The relative paucity in diversity of
studies is probably due to the public health sector's clinic-based, physician controlled
program approach, the use of private sector; nongovernment organizations, social
marketing, and community based distribution for the treatment of Parkinson’s
disease should have been adopted and supported more vigorously if targets were
population is high. This, however, could have been made possible if there was strong
political will and priority given to herbal medicinal treatment of Parkinson’s disease
programs in Nigeria. Parkinson’s disease has had a major impact in countries like
Indonesia, Sri Lanka and Malaysia, which has been attributed to early presidential
support and the continued commitment of national and local leaders should strong
and aggressive focus on herbal treatment of Parkinson’s disease program in Nigeria
will not only reduce mortality rate but also reduce the increased physical and
psychological morbidity effects on the quality of life associated with the
complications of Parkinson’s disease.
2.10 SUMMARY

In summary, it shows there is abundant information about Parkinson’s disease and its
orthodox treatment and awareness which is high among the Nigerian population, but
this awareness has not translated into increased Parkinson’s disease treatment using
herbal medicine, with the end being very low knowledge for herbal treatment of
Parkinson’s disease prevalence in Nigeria. This low Parkinson’s disease herbal
treatment prevalence correlates with high levels of increased physical and
psychological morbidity effects on the quality of life associated with the
complications of Parkinson’s disease, leading to increase in the rural area and in
Nigeria as there are no effective results from the intervention of orthodox
medications. The medical technology is known, and the socio-cultural, religious,
African traditional, traditional practitioners and ancestral dominant factors
impending herbal use in Nigeria. Societies have all been identified, but what is lacking
is the generation of political priority for herbal treatment preservations and
improved invested knowledge as well as the political will and commitment to make
this change on a large scale, as occurred in countries like Malaysia, Sri Lanka, china
Indonesia etc . With the commitment of financial and human resources as well as
assistance from international organizations, public-private sector collaboration,
community-oriented knowledge, acceptability, and wide range of herbal medicinal
treatment choices, the herbal medicinal treatment of Parkinson’s disease prevalence
rate will increase and this should contribute to the reduction of the worst physical
and psychological morbidity effects on the quality of life associated with the
complications of Parkinson’s disease in Africa.
CHAPTER THREE

METHODOLOGY

3.0 PROFILE OF THE STUDY AREA

The study area covers a large part of Amuwo-Odofin, Lagos State. Amuwo-Odofin

LGA is divided into Oriade and Amuwo Local Council Development Area (LCDA) with 7

wards each; Abule-osun, Agboju, Ibeshe, Ijegun, Irede, Kirikir and Kuje wards

constitute Oriade LCDA and Ado-soba, Ekoakete, Ifelodun, IladoTamaro, Irepodun,

Odofin and Orire wards comprising Amuwo LCDA.

Spread among the 14 wards are 67 communities, 12 of which are Urban, 8 semi-

urban and 47 rural. AmuwoOdofin LGA has a population density of approximately

300,000 people per square kilometer.

The LGA, with a population of over 1,500,000 according to the 2006 Census shares its

boundaries with Ajeromi and Ifelodun LCDA in the East, Oriade LCDA in the West, the

Badagry Creek to the South and Isolo/Igando LCDA to the North.

The study of population are the indigenous dwellers of Amuwo-Odofin mainly the

Aworis(Yoruba)comprising also of the Igbos’ and Hausas' etc. However, the Aworis

ethnic group owned the land and are in the majority. They are predominantly farmer,

petty traders, artisan, white collar job workers and a large number of retirees

etc.Some of which are Christians and Muslim dominated with few traditional

worshipers whose festivals are embraced by the people are Elegba, Oro, Sangbeto
and Igunuko. The custodians of culture and tradition in the area are the traditional

rulers. The Local Government is blessed with highly reputable Obas and Chiefs and

Baales. This includes Oba MobadenleObaladeOyekan- the Onilado of Ilado/Inagbe

Islands and Oba Lateef Olayinka Ado, Fabuwa 1, Alado of Ado Land

There are many health facilities, which are made up of hospitals, clinics and

maternity homes.

The analysis in this study was limited to women in their reproductive age.

3.1 STUDY METHODS AND DESIGN

This research work is intended to reveal more on the use of herbal medicine in
the treatment of Parkinson’s disease from the view of non-orthodox medicinal
practitioners in Amuwo-Odofin Local Government Area, Lagos State by interviewing
over 600 NONOTHORDOX MEDICINAL PRACTITIONERS comprising of traditional
medicine practitioners, herbalists, herb sellers and the elderly to encourage the
cultivation and proper documentation of some of the plants which may become
endangered over long use

Prospective method and cross- sectional study was used as the study design.

3.2 DATA COLLECTION TECHNIQUES AND TOOLS

The data collection technique used was interview; the instrument used is

questionnaire containing close and open-ended questions.

3.3 STUDY POPULATION

The study populations were, herbalists , herb sellers and the elderly out of

which are males and females age from 28- 70years. The population is heterogeneous.

3.4. STUDY VARIABLE

The dependent variable was contraceptive use among women.
The independent variables were
* Educational level of respondents
* Religion of respondents
* Attitudes of health providers
* Cultural beliefs of respondents
* Misconception against the use of contraceptives
* Occupation of respondents etc.

3.4 TABLE OF STUDY VARIABLES

Variable Operational Definition Indicator Scale of Technique

measurement
Sex Male Ordinal scale Interview

Female
Occupation Daily work done Herbalist Ordinal scale Interview

Herb-seller

Traditional
 Medical
practitioners
Academic Level of education Tertiary, Ordinal scale Interview
background
Post-

Secondary

Secondary,

Primary

Illiterate
Religion As stated by participant Christian, Islam Ordinal scale Interview
African
Traditional
Others
Age Age as at last birth day 11-20 Ordinal scale Interview
21-30
31-40
41-50
51-60
61 And Above
Knowledge Ever heard & benefit of Yes Nominal Interview
OF family planning Have
No
Parkinson’s you heard about
DISEASE Parkinson’s disease
sources of source Ancestral Ordinal scale Interview
knowledge in
herbal Training
treatment

Ancestral and
 training

Others
areas plants location In the forest Ordinal scale Interview
can be found
in the study only
area
Other places

(Market,

around the

house)
treatment Availability Responses to Ordinal scale Interview
availability questions
asked

knowledge of If any other useful herb Yes Nominal Interview

other herbal
No
treatment

How often Responses to Irregular Ordinal Interview

do you scale
Occasionally
treat questions asked
Parkinson’s
disease Others
Parkinson’s
local names Omisinmisin Leaves Ordinal Interview
of the plant scale
Atare Seed
and the
plant parts Ayunrebonabona
used for Leaves
treating Alubosaelewe
Parkinson’s Leaves
disease Ewe ela Leaves
Oniyemiye Leaves
Iyereosun Leaves
Eso Leaves
Eeran Whole plant
Imo ope Leaves
Ewe iranje Leaves,
root
Lapalapa Fruits
Esisi Leaves, root
Ogede agbagba
Leaves
Ogedewewe Fruits
Igionifon Stem bark
Iyere Leaves, fruit
Werepe, fruit
Taba ewe , leaves
ata ile, root
ewe Asala, leaves
Atareaja Seed
Duration of 2 -3 weeks Ordinal Interview
treatment scale
3 – 5 weeks

5 – 12 weeks

> 12 weeks
Accompani Yes Nominal Interview
ed verbal No
instructions
side effects List out Responses to Ordinal Interview
of some of question asked scale
the herbal
treatment
Will you If there is any doubts Yes Nominal Interview
prefer to
NO
use herbal
medicine to Don’t know
treat
Parkinson’s
disease
If herbal Is there an assurance Yes Nominal Interview
medicine
NO
will take
care of Don’t know
Parkinson’s
disease
What other Massage Ordinal Interview
treatment scale
do you use Diet
apart from
herbs
Animal parts

Divination/Oracle/In

cantation

None

Income more than Ordinal Interview

scale
100k/month
 N50-90k/month

Less than

N50k/month
Marital Married Ordinal Interview
Status scale
Widowed

Single
Knowledge signs and symptoms Shaking hands Ordinal Interview
of the signs scale
and Would not be able
symptoms
of to work well
Parkinson’s
Will be filling tired

Will have pain

Will have poor

memory

3.5. SAMPLING TECHNIQUE

3.5.1 Selection of LGA secretariats , specific residence of herbalists and the elderly,

association of Traditional Medicinal Practitioners and herb sellers market place who
had knowledge about the medicinal uses of plants to represent the whole of

Amuwo-odofin Local Government Area.

3.5.2. Selection of Participants

Participants for the focus groups were selected with the assistance of some key

informants in the LGA secretariats and Traditional Medicinal Practitioners association

through systematic sampling technique, double sampling technique was also adopted

to get sub sample for further information.

In each focus group, I used systematic sample method, out of 30; I used 1 in 3 to get

my 10. For the sub-sample I used simple random technique by writing numbers in

paper and fold and another empty paper without number for the respondents to

pick, to get my 42 altogether.

3.6. SAMPLE SIZE ESTIMATION

A total of eligible 160 candidates were selected from the LGA secretariats in the

community which consisted of 70 Traditional medical practitioners , 50 herb seller,

out of which, 47 participant were selected from (14)market places,28 herbalist from

some specific residence of herbalists given and 15 elders from the LGA, totaling 160.

Out of the 160, 42 volunteer were chosen again through simple random technique

for further information and feedback.

3.7. Data Handling

Filled questionnaire were numbered and checked for completeness, clarity and

consistency at the end of interview. The safety of data collected was guaranteed by

ensuring proper handling and maintaining data. All the data were retrieved and kept

at a secure location to prevent data from adverse weather conditions and domestic

damage.

3.8 Data Analysis

Data collected was summarized and stored in percentages and frequency

distribution tables, which was used to group sample data.

3.9 Statistical Method

Computer software's such as excel was used to create the database.

3.10. Ethical Consideration

Informed consent was sought from LGA secretariats and TCM Association group

in various locations. This enabled me explain the purpose of the study to them,

health issues and preservation of herbal medicinal knowledge and progress are very

sensitive within the traditional setup.

At the same time, conscious efforts were made to learn certain rules that apply to

community before proceedings. All information that is gotten from the participants

was treated as confidential.

3.11 ASSUMPTIONS

: It was assumed that;

(a) The study population was representative of the total population.

(b) The community under study would be receptive and the information given by the

participants were true.

(c) The participants understood the questionnaire due to verbal translation rendered

because most understood and responded in vernacular.

(d) No chieftaincy or tribal conflict within the data collection period, hence reducing

to a large extent the element of bias in the collection of the data.

(e) All quality control measures were strictly adhered to by the researcher.

3.12. Limitation

1. Language barrier may serve as a limitation to the research, since I would not be in

the position to communicate directly with the respondents especially the Hausa

spoken by them, might have led to misunderstanding or misinterpretation of the

important set questions and therefore led to inaccurate results. Although these
limitation was curtailed to a minimum through interpreters who translated the

questions into various language spoken in the community and there was a close

monitoring of the data collected.

2. The one hundred and sixty sample size may not have been a good ground for

extrapolation or generalization of study findings as 600 was intended.

CHAPTER FOUR
4.0. RESULTS
Ages of participants varied greatly, with majority of them coming from the age
range of31-40(43.75%), 41-50(29.37%), 21-30 (17.5%), 51-60 (6.25%) and with a
minority age group of 61 and Above (3.12%) respectively.
The participants on occupation level are made up of about (55%) of Traditional
medical practitioners, (29.37%) are herbalist, (12.5% )are herb-sellers and a minority
of participants are the elderly which are about (3.125%) who could be classified as
the unemployed.
From the table it is also realized that, a total of (50%) believed in Christianity, 43.75%
are practicing Islamic religion, (4.38%) were traditional worshippers and (1.87%) said
they were pagans.
Majority of the participants interviewed are about (56.25) married, (18.75%) single,
(15.625%) are widowed and a minority are divorced (9.375)
On educational level, the minority participants are 10% illiterates, (12.5%) have
primary education, (26.25%) have secondary school education, (13.75) have Post-
Secondary education and majorities have (37.5%) tertiary form of education.
As can be seen from table 1 for their income (63.75%) receive more than
100k/month, about (31.25%) receive N50-90k/month and a minority receive of (5%)
less than N50k/month.

The sexes of the participants are a majority of (61.875%) women and the minority are
(38.125%) men.

Table 1 Demographic Characteristics of Respondents

VARIABLES CATEGORY FREQUENCY PERCENTAGE
(%)
Age
21-30 28 17.5
31-40 70 43.75
41-50 47 29.37
51-60 10 6.25
61 and Above 5 3.12
Total 160 100
OCCUPATION
 Herbalist 47 29.37
Herb-seller 20 12.5
Traditional medical 88 55
practitioners
Elderly 5 3.13
Total 160 100
Religion
Christian 80 50
Islam 70 43.75
African Traditional 7 4.38
Pagan 3 1.87
TOTAL 160 100
MARITAL
STATUS
Married 90 56.25
Single 30 18.75
Widowed 25 15.625
Divorced 15 9.375
TOTAL 160 100
Academic
background
Tertiary 60 37.5
Post-Secondary 22 13.75
Secondary 42 26.25
Primary 20 12.5
Illiterate 16 10
TOTAL 160 100
Income
 More than 102 63.75
100k/month
N50-90k/month 50 31.25
Less than 8 5
N50k/month
TOTAL 160 100
Sex
Male 61 38.13
Female 99 61.88
TOTAL 160 100

4.1 Table 2. Distribution of participants who have heard about Parkinson’s

disease

Have you heard about Parkinson’s Frequency Percentages

disease
Yes 129 80.62
No 31 19.38
TOTAL 160 100

From the table 2, it is observed that knowledge about Parkinson’s disease was
relatively high among the participants, with a proportion of 80.62% having heard of
Parkinson’s disease, this can partly be attributed to the aggressive Parkinson’s
disease campaigns on electronics media and other source, 19.38% however, had
never heard of any Parkinson’s disease.
4.2.0 Table 3. What participants know about the signs and symptoms of
Parkinson’s disease.
 Knowledge of Parkinson’s Frequency Percentage
disease
Shaking hands 100 62.5
Would not be able to work well 17 10.62
Will be filling tired 7 4.38
Will have pain 2 1.25
Will have poor memory 34 21.25
TOTAL 160 100

To find out the depth of knowledge participants had on Parkinson’s disease. 62.5%
said, Parkinson’s disease symptom and sign is Shaking hands, 10.62% said the patient
Would not be able to work well, 4.38% said the patient Will be filling tired, 21.25%
said Will have poor memory, and a minority 1.25% said, Will have pain.
Findings from the above reveal that, a large proportion of the respondents (62.5%)
had more Knowledge of Parkinson’s disease symptom an sign (Shaking hands) so did
21.25% (Will have poor memory).
In order to further investigate into the extent of peoples knowledge about
Parkinson’s disease within the community, a focus Group Discussion session was
organized to determine participant’s knowledge base on Parkinson’s disease, among
others variables; the following were some of their responses.
4.2.1. Knowledge about Herbal treatment for Parkinson’s disease
To determine the participant’s knowledge about Parkinson’s disease, findings
from all focus Group Discussion session conducted within the community was that;
there are herbal treatments for Parkinson’s disease.
4.3. Table 4. Distribution participants who know Herbal treatment for
Parkinson’s disease
Do you know any Herbal Frequency Percentage
treatment for Parkinson’s disease (%)
Yes 102 63.75
No 58 36.25
TOTAL 160 100

From the above table 4, it is realized that 63.75% of those interviewed indicated their
Knowledge on herbal treatment for Parkinson’s disease, 36.25% said they have no
Knowledge on herbal treatment for Parkinson’s disease.
Also, finding from focus group discussion reveal that, a large number of the
participants have Knowledge on herbal treatments cause they are experienced in the
treatment of Parkinson’s disease with herbs. The minority reasons for not knowing
about any herbal medicinal treatment for Parkinson’s disease is as a result of the lack
of knowledge of Parkinson’s disease so they have no idea of its herbal treatment .
4.4 Table 5. Distribution of participants who have treated anyone with
Parkinson’s disease.
Have you ever treated Frequency Percentage %
anyone with Parkinson’s
disease
Yes 102 63.75
No 58 36.25
TOTAL 160 100

From table 5 above, 63.75% of those interviewed indicated said they have treated
Parkinson’s disease, 36.25% participants have never treated Parkinson’s disease. The
reason given by the majority that said “yes” was that they have treated Parkinson’s
disease before while that of the minority that said “No” was because they lack
knowledge of Parkinson’s disease.
4.5 Table 6. Distribution of participants that have treated Parkinson’s disease.
How often do you treat Parkinson’s Frequency Percentage
disease(yes)
Irregular 32 20
Regular 53 33.12
Occasionally 25 15.63
Others 8 5
TOTAL 160 100

From table 6 above, it is observed majority 33.12% treat regularly, 20% treat
irregularly, 15.63% treat occasionally, 5% treat once in a year.
4.6 Table 7: Distribution of participants who have treated Parkinson’s disease
should give names of the plant and the plant parts used for treating Parkinson’s
disease.
The local names of the plant and Frequency Percentages
the plant parts used
Omisinmisin Leaves 1 0.63
Atare Seed 1 0.63
Alubosaelewe Leaves 1 0.63
Ayunrebonabona Leaves 1 0.63

Ewe ela Leaves 1 0.63

Oniyemiye Leaves 1 0.63
Iyereosun Leaves 1 0.63
Eso Leaves 1 0.63
Eeran Whole plant 1 0.63
Imo ope Leaves 1 0.63
Ewe iranje Leaves, root 1 0.63
Lapalapa Fruits 1 0.63
Esisi Leaves, root 1 0.63
Ogede agbagba Leaves 1 0.63
Ogedewewe Fruits 1 0.63
Igionifon Stem bark 1 0.63
Iyere Leaves, fruit 1 0.63
Werepe, fruit 24 15
Taba ewe , leaves 24 15
ata ile, root 24 15
ewe Asala, leaves 24 15
Atareaja Seed 47 29.38
Total 160 100

Majority of 29.38%listed Atareaja Seed others close had similar list of( 4) 15%while
minority listed under of %0.63 listed plants Omisinmisin Leaves, Atare Seed,
Ayunrebonabona Leaves’ Alubosaelewe Leaves, Ewe ela Leaves, Oniyemiye
Leaves,Iyereosun Leaves,Eso Leaves, Eeran Whole plant, Imo ope Leaves, Ewe iranje
Leaves & root, Lapalapa Fruits, Esisi Leaves & root, Ogede agbagba Leaves,
Ogedewewe Fruits, Igionifon Stem & bark, Iyere Leaves & fruit.
4.7 Table 8. Distribution of those if they be aware of other treatment which will
be useful for Parkinson’s disease.
Are you aware of other Frequency Percentages
treatment which will be
useful
Yes 102 63.75
No 58 36.25
TOTAL 160 100

When participants were asked to find out about those who are aware of other
treatment which will be useful the ones who said “yes” are 63.75% while those that
said “No” to being aware of other treatment which will be useful 36.25%.

4.8 Table 9. Distribution of participants who knew other treatment used apart
from herbs

What other treatment do you Frequency Percentages

use apart from herbs
Massage 70 43.75
Diet 58 36.25
Animal parts 4 2.5
Divination/Oracle/Incantation 18 11.25
None 10 6.25
Total 160 100

When participants were asked whether they knew other treatment asides herbs
,majority 43.75% said massage , 36.25% said diet, 11.25%
Divination/Oracle/Incantation, 6.25% said None, the minority 2.5% said Animal
parts.
4.9. Table 10. Distribution of participants who think herbal medicine will take care
of Parkinson’s disease.
Do you think herbal medicine will take care of Frequency Percentages
Parkinson’s disease
Yes 102 63.75
No 0 0
Don’t know 58 36.25
TOTAL 160 100

When participants were asked if they think herbal medicine will take care of
Parkinson’s disease.
63.75% said “Yes”, 36.25% said they don’t know because they haven’t heard of
Parkinson’s disease and for “No” had no one tick.

4.10 Table 11. Distribution of participants that Will prefer to use herbal medicine
to treat Parkinson’s disease
Will you prefer to use Frequency Percentages
herbal medicine to treat
Parkinson’s disease
Yes 160 100
No 0 0
Don’t know 0 0
TOTAL 160 100

A total of 100% representing the majority indicated they will prefer to use herbal
medicine to treat Parkinson’s disease because they were enlightened on how World
Health Organization supports herbal medicine
4.11 Table 12. Distribution of participants on what side effects do some of the
herbal treatment have.

What are the side effects of some of Frequency Percentages

the herbal treatment
None 102 63.75
Nausea and vomiting 58 36.25
Total 160 100

When participants were asked on what side effects some may of the herbal
treatment may have, 63.75% and minority 36.25%said “None”.

4.12 Table 13. Distribution of participants who were asked what duration it took
for the treatment for the patients they treat

What is the duration of Frequency Percentages

the treatment for the
patients you treat
2 -3 weeks 3 1.86
3 – 5 weeks 28 17.5
5 – 12 weeks 44 27.5
> 12 weeks 85 53.13
Total 160 100

When the participants were interviewed on what duration it took for the treatment
for the patients they treat majority 53.13%said > 12 weeks, 27.5% said 5 – 12 weeks,
17.5% said 3 – 5 weeks while the minority 1.86% said 2 -3 weeks.

4.13 Table 14. Distribution of participants were asked if the plants to treat are
readily available.

Are the plants to treat readily available Frequency Percentages

Yes o o
No 102 63.75
Don’t know 58 36.25

TOTAL 160 100

A question was asked if the plants to treat are readily available. A majority 63.75%
said “No” no one said yes their major reasons were weather conditions and 36.25%
said they “Don’t know” cause of their lack of their knowledge of Parkinson’s disease.

4.14 Table 15. Distribution of participants that knew where they can find the
plants in the study area
What areas can the plants be found in Frequency Percentages
the study area
In the forest only 22 13.75
Other places (Market, around the house 138 86.25
TOTAL 160 100

86.25% said the plants can be found in other places (Market, around the house I the
study area while 13.75% said in the forest only.

4.15. Table 16. Distribution of participants were asked what their sources of
knowledge in herbal treatment was from
What are your sources of knowledge in herbal Frequency Percentages
treatment
Ancestral 10 6.25
Training 100 62.5
Ancestral and training 28 17.5
others 22 13.75
TOTAL 160 100

Majority of the participants 62.5% got Training knowledge in herbal treatment ,

17.5% got both Ancestral and training knowledge in herbal treatment , 13.75% got
university knowledge in herbal treatment and a minority got Ancestral knowledge in
herbal treatment.

4.16. Table 17. Distribution of participants that were asked if they give verbal
instructions during treatment
Do you give verbal instructions Frequenc Percentages
during treatment y
Yes 107 66.88
No 53 33.12
TOTAL

Participants were asked if they give verbal instructions during treatment and a
majority of 66.88% said “yes” while minority said “no” because they have no
knowledge of Parkinson’s disease.