Herbal Medicines in the Management of
Migraine:
Ethnobotanical Insights and Pharmacological
Perspectives
R. Saraswathi1, S. Anbazhagan2,
P. Muralidharan3*
1Department of Pharmacology, Chettinad Academy of
Research and Education, Kelambakkam - 603103.
2Department of Pharmaceutical Chemistry, Surya School
of Pharmacy, Villupuram - 605652.
3Professor, Department of Pharmacology, Chettinad
School of Pharmaceutical sciences, Chettinad Hospital and Research Institute,
Chettinad Academy of Research and Education, Kelambakkam - 603103, Tamilnadu,
India.
*Corresponding Author E-mail:
muralidharanp@care.edu.in
ABSTRACT:
Background: Migraine is a complex and recurrent neurovascular
disorder that significantly impacts the quality of life and productivity of
individuals worldwide. The limitations of conventional pharmacological
therapies, including adverse effects and variable efficacy, have fuelled
growing interest in herbal medicines as alternative or adjunct treatment
options. Objective: This review aims to systematically explore
and evaluate medicinal plants traditionally used for migraine management, with
a focus on ethnobotanical origins, active phytoconstituents, mechanisms of
action, and pharmacological validation. Methods: An extensive literature
search was conducted using scientific databases such as PubMed, Scopus, and Web
of Science to identify ethnomedicinal reports and experimental studies (in
vitro, in vivo, and clinical trials) related to herbal treatments for migraine.
Results: Numerous medicinal plants—including Tanacetum
parthenium (feverfew), Petasites hybridus (butterbur), Zingiber
officinale (ginger), and Mentha piperita (peppermint) etc.,
demonstrate antimigraine activity through diverse pharmacological actions such
as anti-inflammatory effects, serotonergic modulation, CGRP inhibition,
antioxidant activity, and vasodilation. The bioactive compounds implicated
include sesquiterpene lactones, flavonoids, alkaloids, and essential oils. Conclusion:
Herbal medicines present a promising and multifaceted approach to migraine
management, drawing from rich ethnobotanical traditions and supported by
emerging pharmacological evidence. However, further clinical validation,
standardization of formulations, and mechanistic studies are essential to
ensure their efficacy, safety, and integration into modern therapeutic
regimens.
KEYWORDS: Migraine, Herbal medicines, Ethnobotany,
Phytotherapy, Medicinal plants and Phytochemicals.
INTRODUCTION:
Migraine is a prevalent and complex neurological
disorder characterized by acute, chronic, multifactorial, disabling, and
recurrent neurovascular headaches with a strong hereditary component.
Typically, it begins in childhood with a few episodes per year and progresses
in frequency to several attacks per week in adulthood, with a higher prevalence
observed in females. Migraine attacks are often preceded by prodromal symptoms
and aura—transient focal neurological disturbances believed to originate from
dysfunctions in the hypothalamus, brainstem, and cerebral cortex. The headache
phase is commonly unilateral, pulsatile, and exacerbated by routine physical
activity. It is frequently accompanied by nausea, vomiting, photophobia,
phonophobia, osmophobia, cutaneous allodynia, and muscle tenderness. These
manifestations reflect widespread abnormalities in multiple neuronal systems
throughout the course of a migraine attack. Pathophysiologically, migraines are
associated with spontaneous hyperactivity and heightened sensitivity in pain
and other predominantly sensory pathways within the brainstem. Furthermore,
individuals with migraine are at an increased risk of cerebrovascular and
cardiovascular events, such as stroke and myocardial infarction. The duration
of an episode can range from a few hours to several days, substantially
impairing quality of life.1
Migraine ranks as the third leading cause of
disability among individuals under 50 years of age, affecting both males and
females.2 Despite advances in pharmacological therapies, many
patients continue to struggle with treatment due to issues related to
tolerability, accessibility, or cost. The term “migraine” is derived from the
Greek word hemikrania, meaning “half of the head,” reflecting one of
the hallmark characteristics of the disorder-pain that often localizes to one
side of the head in a significant number of cases.3
Migraine
without Aura:4
Migraine is a persistent headache disorder
with episodes lasting between four to seventy two hours. The condition
typically presents with unilateral head pain of a pulsating nature, which can
vary in intensity from mild to severe. The headache is often aggravated by
routine physical activity and is commonly accompanied by associated symptoms
such as nausea, photophobia, and phonophobia.5
Migraine
with aura:4
Migraine with aura is characterized by recurrent
attacks featuring fully reversible visual, sensory, or other central nervous
system symptoms, typically unilateral and lasting for several minutes. In most
cases, these symptoms appear gradually and headache and other migraine symptoms
follow. In children and adolescents, atypical bilateral visual symptoms may
occur, which could represent an aura.5
Classic Migraine:5
Migraine with aura is defined by the presence of
sensory, visual, and/or speech or language disturbances, occurring individually
or in combination, without accompanying motor weakness. These symptoms
typically evolve gradually, display both positive and negative features,
persist for no more than one hour per symptom, and are fully reversible.
·
Typical aura with headache: A migraine with typical aura is
characterized by either with or without migraine and followed within 60
minutes.
·
Typical aura without
headache: This type is
neither accompanied nor followed by any kind of headache.
Basilar Migraine:
Migraine without
motor weakness that has aura symptoms that are originating from brainstem.
Hemiplegic Migraine:
Migraine
with aura which includes the
motor weakness.
·
Familial hemiplegic
migraine (FHM): Migraine
with aura includes motor weakness, and at least one first- or second-degree
relative who has migraine aura with motor
weakness.
·
Sporadic hemiplegic
migraine (SHM): Migraine with aura includes motor
weakness is not seen in any first-
or second-degree relatives.
Retinal
Migraine:5
This involves repeated episodes of visual
disturbances in a single eye such as scintillations, scotomata, or transient
blindness—that occur in association with migraine headaches.
Chronic Migraine:
Headache occurring on
fifteen or more days each month for a duration of more than three months, with
migraine-like symptoms present on at least eight of those days per month.
Complications of Migraine:
1. Status migrainosus: A crippling migraine attack that lasts more than seventy-two hours.
2. Persistent aura without infarction: Aura symptoms that lasts for one or more
weeks without neuroimaging showing signs.
3. Migrainous infarction: This refers to one or more migraine aura
symptoms that start during normal migraine with aura episodic and are linked to
an ischemic brain lesion in the relevant area demonstrated by neuroimaging.
4. Migraine aura triggered seizure: This type of seizure is the result of an
aura-accompained migraine attack
Probable migraine
Migraine-like episodes that lack one of
the necessary features to fully meet the criteria for any specific type or subtype
of migraine listed above, and not fulfill the diagnostic criteria for any other
headache disorder.
1.
Probable migraine
without aura.
2.
Probable migraine with
aura.
Episodic Syndromes with Migraine Recurrent
GI Disturbance:
Recurrent episodic of abdominal pain
and/or discomfort, along with nausea and/or vomiting, that occur occasionally,
persist over time, or happen at regular intervals and may be linked to migraine.
·
Cyclic vomiting
syndrome: These are repeated, episodic attacks with
severe nausea and vomiting, that usually follow a consistent pattern to each
individual and tend to occur at regular, predictable intervals. These episodes
may also include symptoms like pallor and fatigue, with a complete absence of
symptoms between episodes.
·
Abdominal migraine: This idiopathic disorder is marked by repeated
episodes of moderate to severe abdominal pain centered around the midline, most
commonly in children. This pain is accompanied by vasomotor symptoms, nausea,
and vomiting, with each episode lasting from two to seventy-two hours. The
intervals between episodes are free of symptoms, and headache are absent during
the attacks.
Benign Paroxysmal Vertigo:
This disorder is characterized by repeated
short episodes of vertigo that occur suddenly and resolve on their own,
typically affecting otherwise healthy children.
Benign Paroxysmal Torticollis:
This condition involves recurrent episodes
of head tilting to one side, sometimes accompanied by slight rotation which
resolve on their own. It typically occurs in infants and young children, with
onset usually within the first year of life.5
DIAGNOSIS:5
Diagnostic criteria for migraine without
aura (Common Migraine)
A.
A minimum of five
attacks that fulfilling criteria B-D
B.
Headache episodes
lasting between 4-72 hrs. (When untreated
or unsuccessfully treated)
C.
The headache must have
at least two of the following four features:
1.
Pain localized to one
side of the head (unilateral)
2.
Throbbing or pulsating
in nature
3.
moderate to severe intensity of pain
4.
Worsening with or
leading to avoidance of routine physical activity (such as walking or climbing stairs)
D.
During headache at least one of the following:
1.
nausea and/or vomiting
2.
photophobia and phonophobia
E.
Not better accounted for by another
ICHD-3 diagnosis
Diagnostic criteria
for migraine with aura (Classic
Migraine)
:
A. A minimum of two attacks must meet the
requirements of both criteria B and C
B. One or more of the following fully
reversible aura symptoms
may be present: Visual, sensory, speech and/or language, motor, brainstem, or retinal
C. At least
three of the following six characteristics:
1. at least one aura symptom
spreads gradually over ≥5 minutes
2. two or more aura symptoms occur in succession
3. each individual
aura symptom lasts 5-60 minutes
4. at least
one aura symptom is unilateral
5. at least one aura symptom
is positive
6. the aura is accompanied, or followed within 60 minutes,
by headache
D. Not more
accurately explained by another ICHD-3 diagnosis
Causes:6
A migraine is believed to result
from abnormal brain activity, although the precise pathophysiological
mechanisms remain incompletely understood. Current evidence suggests that
migraine attacks originate within central nervous system and involve complex
interactions among neural pathways, neurotransmitter imbalances, and
alterations in cerebral blood flow. These events may contribute to the
initiation and progression of migraine symptoms. While the exact etiology
remains elusive, several hypotheses have been proposed, including:
·
A central nervous system disorder that predisposes individuals to
migraine episodes.
·
Dysregulation of cerebral vascular function contributing to symptom
onset.
·
A genetic predisposition increasing susceptibility to migraines.
·
Imbalances in neurotransmitters and aberrant nerve signalling
triggering attacks
Table: 1 Common Triggers of Migraine1-5
|
Category
|
Examples /
Description
|
|
Hormonal
|
Menstruation,
pregnancy, menopause, hormonal contraceptives
|
|
Emotional
|
Stress, anxiety,
depression, emotional disturbances
|
|
Physical
|
Fatigue, sleep
disturbances, physical exertion, poor posture
|
|
Dietary
|
Skipped meals,
dehydration, caffeine, alcohol, chocolate, aged cheese, processed meats
|
|
Genetic
|
Family history of
migraine, inherited susceptibility
|
|
Environmental
|
Bright lights,
loud noises, strong odors, weather or altitude changes
|
|
Medicinal
|
Oral
contraceptives, vasodilators, hormone replacement therapy, certain analgesics
|
Figure 1:
Migraine trigger and their percentage of contribution1-5
SYMPTOMS:7- 10
Table: 2 Migraine Symptoms by Stages
Premonitory Phase or Prodrome
|
Aura Phase
|
Pain Phase
|
Postdrome Phase
|
|
Irritability
|
Visual disturbance
|
Throbbing
|
Inability to
concentrate
|
|
Yawning
|
Temporary loss
of sight
|
Drilling
|
Fatigue
|
|
Mood Changes
|
Numbness and tingling on part of body
|
Ice pick in the
head
|
Depressed mood
|
|
Increased need to urinate
|
Difficulty in
speaking
|
Burning
|
Euphoric mood
|
|
Food cravings
|
|
Nausea
|
Lack of comprehension
|
|
Sensitivity to Light/
Sound
|
|
Vomiting
|
|
|
Fatigue
|
|
Anxiety
|
|
|
Muscle stiffness
|
|
Depression
|
|
|
Nausea
|
|
Sensitivity to light/sound
|
|
Phases of Migraine:
Figure 2. Phase of migraine7-10
(A. Prodrome,
B. Aura, C. Headache and D. Postdrome)
Historical Perspectives:
The vascular theory of
migraine, first proposed by neurologist Dr. Harold G. Wolff in
the 1940s, marked a pivotal development in understanding migraine
pathophysiology. According to this theory, migraine attacks are initiated by a transient vasoconstriction of
cerebral blood vessels, leading to cerebral
oligemia and the onset of aura symptoms. This phase is subsequently followed by a
reactive vasodilation
of intracranial or extracranial arteries, which Wolff postulated as the primary
mechanism responsible for the headache
phase of the migraine attack11. Wolff emphasized the
idea that "all pain is an action
violated," suggesting that arterial dilation, particularly of the meningeal and cerebral vessels, was
the principal source of migraine pain.12 While the brain parenchyma
itself is largely devoid of nociceptors, the dura mater and its associated vessels are richly
innervated by the trigeminal nerve,
rendering them highly pain-sensitive. The dilation of these vessels was
hypothesized to stimulate perivascular
trigeminal afferents, resulting in the pulsatile pain
characteristic of migraines. However, subsequent clinical and neuroimaging
investigations revealed significant
inconsistencies between vascular changes and migraine
symptomatology. In many cases, vascular
alterations did not correspond temporally or in magnitude with
the clinical manifestations of migraine. These discrepancies gave rise to skepticism
regarding the vascular origin
of migraine and led to the development of alternative hypotheses, most notably
the neurogenic theory.13
Pathogenesis of Migraine:8-15
Migraine is a multifaceted neurovascular condition marked by recurring
headaches accompanied by sensory change. Its pathogenesis involves the dynamic
interplay between neuronal hyper
excitability, cortical
spreading depression (CSD), trigeminovascular system activation,
and neurogenic inflammation.
CSD, particularly associated with migraine aura, initiates a cascade that
activates the trigeminal afferents,
leading to the release of vasoactive
neuropeptides such as calcitonin gene-related peptide (CGRP),
substance P,
and neurokinin A.
These neuropeptides induce vasodilation,
plasma protein extravasation,
and mast cell degranulation,
contributing to neurogenic
inflammation and nociceptive
transmission. Sustained activation results in central sensitization,
enhancing pain perception and contributing to symptoms like cutaneous
allodynia. Brainstem nuclei
(e.g., periaqueductal gray, locus coeruleus) and the hypothalamus are involved in
modulating pain and autonomic responses, and may serve as migraine generators.
Additionally, serotonergic
dysregulation, genetic
predisposition, and pro-inflammatory cytokines further
exacerbate susceptibility and chronicity. Among these, CGRP has emerged as a
key molecular target, and its antagonism has shown promising therapeutic
outcomes. These insights underpin the development of targeted pharmacological
interventions in migraine management.
Figure 3:
Pathogenesis of Migraine13
Current Treatments of Migraine16-19
Migraine management involves acute (abortive) therapies to relieve pain
during attacks and preventive (prophylactic) treatments to reduce attack
frequency, severity, and duration.
Non-Pharmacological Approaches:
Lifestyle modifications (such as sleep hygiene, stress management, and
avoiding dietary triggers), along with behavioural therapies, and
neuromodulation techniques (like transcranial magnetic stimulation and vagus
nerve stimulation), complement pharmacotherapy and improve overall outcomes.
Ethnobotanical Overview of Antimigraine Plants:
Numerous cultures have historically used plant
remedies to manage headaches and migraine. Table 3 summarizes some of the most
widely used medicinal plants, their traditional uses, parts used, and
preparation methods.
Table 3. Ethnobotanical review of Antimigraine Plants
|
No
|
Scientific Name
|
Family
|
Parts Used
|
Key Phytoconstituents
|
Types of Migraine Treated
|
Description of Use
|
|
1
|
Tanacetum parthenium
|
Asteraceae
|
Leaves
|
Parthenolide, flavonoids
|
Migraine with/ without aura
|
Traditionally used to prevent migraines by inhibiting
serotonin release and reducing inflammation.20,21
|
|
2
|
Petasites hybridus
|
Asteraceae
|
Roots, leaves
|
Petasin, isopetasin
|
Migraine prophylaxis
|
Extracts reduce migraine frequency; PA-free forms are
essential due to potential liver toxicity.21
|
|
3
|
Scutellaria lateriflora
|
Lamiaceae
|
Aerial parts
|
Baicalin, scutellarin, flavonoids
|
Tension-type headaches
|
Used as a mild sedative; may alleviate headaches
through calming effects.22
|
|
4
|
Viola odorata
|
Violaceae
|
Flowers, leaves
|
Salicylic acid, flavonoids
|
Migraine, tension headaches
|
Employed for its anti-inflammatory and sedative
properties.23
|
|
5
|
Ziziphora clinopodioides
|
Lamiaceae
|
Leaves
|
Essential oils, flavonoids
|
Headaches, migraines
|
Traditional remedy for headaches; possesses analgesic
and anti-inflammatory effects.21,24
|
|
6
|
Echium amoenum
|
Boraginaceae
|
Flowers
|
Rosmarinic acid, flavonoids
|
Tension headaches, migraines
|
Known for its sedative and anxiolytic properties;
used in traditional medicine for headache relief.25
|
|
7
|
Ferula persica
|
Apiaceae
|
Roots
|
Sesquiterpenes, coumarins
|
Sinus-related headaches, migraines
|
Utilized for its anti-inflammatory and analgesic
properties.23,29
|
|
8
|
Fumaria asepala
|
Papaveraceae
|
Whole plant
|
Alkaloids, flavonoids
|
Migraines
|
Traditionally used as a sedative and for its
hypotensive effects.26
|
|
9
|
Heracleum persicum
|
Apiaceae
|
Seeds, roots
|
Furanocoumarins, essential oils
|
Sinus headaches, migraines
|
Employed for its anti-inflammatory and analgesic
properties.26
|
|
10
|
Nigella sativa
|
Ranunculaceae
|
Seeds
|
Thymoquinone, nigellone
|
Hypertension-related headaches
|
Used to manage headaches linked to hypertension;
possesses anti-inflammatory effects.25,27
|
|
11
|
Ocimum basilicum
|
Lamiaceae
|
Leaves
|
Eugenol, linalool
|
Tension headaches, migraines
|
Known for its analgesic and muscle relaxant
properties.28
|
|
12
|
Citrus aurantium
|
Rutaceae
|
Peel, flowers
|
Flavonoids, essential oils
|
Migraines
|
Utilized for its calming and sedative effects.
|
|
13
|
Cinnamomum zeylanicum
|
Lauraceae
|
Bark
|
Cinnamaldehyde, eugenol
|
Migraines
|
Employed for its anti-inflammatory and analgesic
properties.28
|
|
14
|
Salix alba
|
Salicaceae
|
Bark
|
Salicin
|
Migraines, general headaches
|
Source of salicin, a precursor to aspirin; used for
its analgesic effects.30
|
|
15
|
Anisodus tanguticus
|
Solanaceae
|
Roots
|
Hyoscyamine, scopolamine
|
Vascular migraines
|
Contains anticholinergic alkaloids; used in
traditional Chinese medicine for migraines.31
|
|
16
|
Mirabilis jalapa
|
Nyctaginaceae
|
Roots, leaves
|
Alkaloids, flavonoids
|
Headaches
|
Traditional use includes treatment for headaches and
inflammation.32
|
|
17
|
Cleome gynandra
|
Cleomaceae
|
Leaves
|
Flavonoids, glucosinolates
|
Headaches
|
Used for its anti-inflammatory and analgesic
properties.26
|
|
18
|
Matricaria recutita
|
Asteraceae
|
Flowers
|
Apigenin, chamazulene
|
Migraines
|
Known for its calming effects; used to alleviate
migraine symptoms.26
|
|
19
|
Piper nigrum
|
Piperaceae
|
Seeds
|
Piperine
|
Migraines
|
Employed for its analgesic and anti-inflammatory
properties.33
|
|
20
|
Brassica nigra
|
Brassicaceae
|
Seeds
|
Glucosinolates, sinigrin
|
Migraines
|
Traditional use includes treatment for headaches and
migraines.34
|
Phytochemicals and Pharmacological Mechanisms35-37
Medicinal plants exhibit antimigraine activity through
several bioactive compounds, such as:
1.
Sesquiterpene
lactones (e.g.,
parthenolide from feverfew): Inhibits NF-κB, reducing inflammation.
2.
Flavonoids (e.g., quercetin): Antioxidant and
vasoprotective actions.
3.
Alkaloids (e.g., caffeine, berberine):
Modulate central neurotransmitters.
4.
Essential oils (e.g., menthol): Local anesthetic
and cooling effects.
Pharmacological studies show that these compounds
modulate serotonergic pathways, suppress CGRP release, and exhibit
anti-inflammatory and antioxidant activities-key mechanisms implicated in
migraine pathophysiology.
Clinical Evidence and Safety Profiles:
While preclinical data are robust, clinical evidence
remains limited but encouraging. Feverfew and butterbur have shown efficacy in
reducing migraine frequency in randomized controlled trials. Ginger has been
found to be comparable to sumatriptan in aborting acute attacks in some
studies. However, issues such as hepatotoxicity (butterbur) and variability in
plant extracts highlight the need for rigorous standardization and regulatory
oversight.
CONCLUSION:
Herbal medicines represent a valuable yet
underutilized resource in the management of migraine, drawing upon centuries of
ethnobotanical knowledge and growing pharmacological evidence. This review
highlights several medicinal plants with documented antimigraine activity,
acting through diverse mechanisms such as serotonergic modulation,
anti-inflammatory pathways, CGRP inhibition, and antioxidant effects. Key
phytoconstituents—such as sesquiterpene lactones, flavonoids, alkaloids, and
essential oils—have shown significant potential in both preclinical and limited
clinical settings. Despite these promising findings, the integration of herbal
therapies into mainstream migraine treatment is hindered by several challenges,
including inconsistent quality of herbal products, limited clinical trials,
variability in dosage and formulation, and lack of standardized guidelines.
Addressing these gaps requires multidisciplinary collaboration to establish
rigorous scientific validation, safety profiling, and regulatory frameworks.
Moving forward, well-designed clinical trials,
phytochemical standardization, and advanced pharmacological studies are
essential to confirm efficacy, elucidate mechanisms, and ensure safe
therapeutic use. Bridging the gap between traditional medicine and modern
science may ultimately lead to the development of effective, affordable, and
patient-friendly alternatives or adjuncts to conventional migraine therapies.
ACKNOWLEDGMENTS:
We are sincerely acknowledged to Chettinad Academy of Research and
Education, Kelambakkam, Kanchipuram, Tamil nadu, for the great support for our
research work.
CONFLICT OF INTERESTS:
We have No conflict interest.
AUTHOR CONTRIBUTIONS:
Equal contribution for all authors
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