Prolonged Hemiplegic Migraine Led to Persistent Hyperperfusion and Cortical Necrosis: Case Report and Literature

Yacen Hu1,2, Zhiqin Wang1,2, Lin Zhou1,2

  • 1Department of Geriatric Neurology, Xiangya Hospital, Central South University, Changsha, China.

Frontiers in Neurology
|November 15, 2021
PubMed

Insights

This case study shows prolonged hemiplegic migraine attacks can cause permanent brain damage. Patent foramen ovale closure significantly reduced attacks in a patient with hemiplegic migraine.

Area of Science:

  • Neurology
  • Neuroimaging
  • Vascular Neurology

Background:

  • Hemiplegic migraine (HM) is a rare migraine subtype with temporary motor weakness.
  • Permanent deficits and imaging changes are uncommon in HM.

Observation:

  • A patient experienced severe, medication-refractory hemiplegic migraine attacks.
  • Attacks led to irreversible visual impairment and cortical necrosis.
  • Multimodal MRI revealed persistent vasodilation and hyperperfusion during attacks.

Findings:

  • Prolonged HM attacks can cause permanent neurological deficits and cortical necrosis.
  • Persistent hyperperfusion may contribute to prolonged attacks and lasting damage.
  • The patient had a patent foramen ovale (PFO).

Implications:

  • Screening for PFO is recommended in patients with prolonged or intractable HM.
  • PFO closure may reduce HM attack frequency and prevent severe sequelae.
  • This case highlights potential mechanisms and management strategies for severe HM.

Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...