1MBBS, MD Psychiatry, Fellowship Palliative Care, Chief Consultant Psychiatrist, Dr Harjot Singh’s Neuropsychiatry Centre and Hospital, India
2MBBS, MD Psychiatry, Professor & Head, Department of Psychiatry, Government Medical College, India
3MBBS, MD Psychiatry, Consultant Psychiatrist, Dr Harjot Singh’s Neuropsychiatry Centre and Hospital, India
4MBBS, MD Psychiatry, Professor & Head, Department of Psychiatry, Sri Guru Ram Das Institute of Medical Sciences and Research, India
Received: March 07, 2025; Published: March 17, 2025
*Corresponding author: Harjot Singh, MBBS, MD Psychiatry, Fellowship Palliative Care, Chief Consultant Psychiatrist, Dr Harjot Singh’s
Neuropsychiatry Centre and Hospital, India
This is a case study on 23year old female having severe unilateral headache with tinnitus, dysguesia and hemiplegia,
who was initially misdiagnosed as dissociative disorder. Detailed history and evaluation reported it to be
a case of complicated migraine with neurological manifestations. Start of migraine prophylaxis showed significant
improvement in symptoms.
Keywords: Abbreviations: CSD: Cortical Spreading Depression; ICHD2: International Classification of Headache Disorders 2; HM: Hemiplegic Migraine
As per Global Burden of Disease 2015, Headache disorders were
collectively the third leading cause of disability in people under 50
years of age. Even though, migrane is second most common type of
headache following tension- type heachadche, the burden of migraine
is much higher affecting over a billion of people worldwide. (Stovner
[1]) The word “migraine” is derived from the Greek word hemikrania,
which was later converted into Latin as hemigrane. Migraine is a
cyclic disorder which has different phases, including a premonitory
phase, transient neurological symptoms (i.e., migraine aura), intense
headache attack and postdrome phase. Migraine can be classified
into two types- migraine with aura and migraine without aura. (Jatin
Gupta, et al. [2]). International Classification of Headache Disorders 2
[ICHD2], 2004, the classified aura into four types:
1. Visual aura, the most common;
2. Sensory aura;
3. Language aura, which occur less commonly;
4. Motor aura, the least common. (Foroozan, et al. [3])
A 23year old female studying abroad came back to India with
complaints of severe headache, she reported she had difficulty in
concentrating in studies, would not come out of the room, keep the
curtains closed, away from any light and sounds. It was also accompanied
by presence of nausea and floaters. These episodes lasted for
almost 3 days. She had taken acetaminophen without any specialist
consultation, reported mild relieve in symptoms. After almost 20
days, she first developed difficulty in breathing and chest pain lasting
for almost 1 hour, it was followed by paresthesia throughout body and
hemiparesis of left side for almost 30 minutes. Pulsating headache on
right side including orbital region continued throughout the day. Next
day morning, along with the symptoms of previous day she had tinnitus
and dysgeusia, which was followed by weakness of one side of
body resulting difficulty bearing weight, developed ptosis and swelling
on one side of face. Patient was first admitted in the tertiary hospital
where the history of the patient revealed stressors and she was
diagnosed with dissociative disorder, was started on antidepressant
and anxiolytics. She reported no improvement in the symptoms, her
conditions continued to worsen over next 5 days. Following this, she
was brought to our hospital, where detailed examination was done.
Past history revealed history of difficulty breathing, followed by
episodes of loss of consciousness. This was followed by unilateral
pulsating headache associated with nausea and vomiting. She was
started on Prothiaden 25mg and Flunarizine 10mg. she took medication
for almost 3-4 months. And was asymptomatic for 1 year. After
1 year, again she developed similar complaints. General physical examination
revealed reduced power, nystagmus and ptosis. Complete
hemogram was normal. Electrocardiography was normal. Electroencephalography
showed lower alpha and beta activity. MRI brain
showed no significant changes. Case discussion with panel of consultants
was done and she was diagnosed with complicated migraine
with neurological manifestations. She was started on intravenous
valproate 250mg twice daily and flunarizine 10mg at night. Combination
of Magnesium and riboflavin was also started. Patient started
to report improvement within 48 hours. Sumatriptan nasal spray
was prescribed, on need basis in case headache develops. Patient was
completely asymptomatic within a week. But she continued to have
dysguesia for almost 1 month. She is coming for follow up for past
three months, with no further episode.
The International Headache Society identifies motor aura as a
hallmark feature of hemiplegic migraine (HM), a specific migraine
subtype characterized by reversible motor weakness. While motor
aura is usually temporary, rare cases exhibit prolonged or even permanent
symptoms, leading to lasting neurological impairments, progressive
cognitive decline, and significant brain MRI changes following
HM episodes. These changes may include a progressive pattern
of brain atrophy. (Arnold [4]) The activation of the trigeminovascular
system is considered the most common neurobiological mechanism
underlying migraine. This activation may result from cortical
spreading depression (CSD) and dysfunction in brainstem nuclei involved
in central pain regulation. Genetics also play a crucial role,
particularly gain-of-function mutations in the SCN1A gene, which
contribute to neuronal hyperexcitability and prolonged depolarization
linked to CSD. (Cest`ele, et al. [5]) The sustained depolarization
of inhibitory neurons leads to chloride ion depletion and extracellular
potassium accumulation, disrupting neuronal equilibrium. This imbalance
may trigger widespread neuronal depolarization, excessive
glutamate release, and the onset of CSD. Prolonged aura and CSD can
increase metabolic demand, potentially causing cortical swelling, contrast
enhancement, and blood–brain barrier dysfunction. (Charles, et
al. [6]) (Pietrobon, et al. [7]).
The transient cortical enhancement observed on MRI in these
cases may be indicative of a disrupted blood–brain barrier—an uncommon
finding in hemiplegic migraine (HM) that could be linked to
the severity of the attack. The irreversible changes in such patients
may be attributed to cytotoxic edema, representing an extreme manifestation
of CSD, ultimately leading to cell death. No evidence of any
specific medication for acute or preventive therapies is available. Only
past case reports have shown the benefits of using nasal ketamine, intravenous
furosemide, magnesium, and verapamil for acute headache
and aura treatment. (Di Stefano, et al. [8]) A case study has shown
potential benefits of valproate in such cases. Our patient also benefited
from the use of valproic acid and flunarizine. (Jokubaitis, et al. [9])
Motor aura being very uncommon can be misdiagnosed, but before
reaching the diagnosis of motor aura all the other possible causes
of hemiplegia should be ruled out. Timely management would result
in prevention of permanent damage in brain.
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