Focal cortical dysplasia type II: biological features and clinical perspectives

Sanjay M Sisodiya1, Susanne Fauser, J Helen Cross

  • 1Department of Clinical and Experimental Epilepsy, UCL Institute of Neurology, Queen Square, London, UK. sisodiya@ion.ucl.ac.uk

The Lancet. Neurology
|August 15, 2009
PubMed

Insights

Focal cortical dysplasia (FCD) type II causes drug-resistant epilepsy. Improved in vivo MRI detection can guide surgical treatment, offering a potential cure for this challenging neurological disorder.

Area of Science:

  • Neurology
  • Neuroscience
  • Medical Imaging

Background:

  • Focal cortical dysplasia (FCD) type II is a significant cause of drug-resistant epilepsy.
  • Diagnosis is challenging due to variable clinical presentations and reliance on histopathology.
  • In vivo identification via MRI is crucial for effective patient management.

Purpose of the Study:

  • To highlight the importance of in vivo MRI for diagnosing FCD type II.
  • To emphasize the impact of accurate diagnosis on treatment strategies.
  • To explore the underlying cellular anomalies and their implications for epilepsy.

Main Methods:

  • Review of clinical presentations and diagnostic challenges of FCD type II.
  • Discussion of the role of MRI in identifying FCD type II lesions.
  • Analysis of histopathological findings and their molecular underpinnings.

Main Results:

  • FCD type II presents variably, often requiring specialist assessment.
  • Surgical intervention can be curative when FCD type II is accurately diagnosed.
  • Cellular anomalies suggest widespread molecular disruption and potential neurodegeneration.

Conclusions:

  • Improved in vivo MRI detection of FCD type II is essential.
  • Accurate diagnosis directs patients towards potentially curative surgical options.
  • Understanding FCD type II mechanisms may offer broader insights into neurological disorders and epilepsy.

Related Concept Videos

Dissociative Identity Disorder01:30

Dissociative Identity Disorder

Dissociative Identity Disorder (DID), previously termed multiple personality disorder, is a complex psychological condition characterized by the presence of two or more distinct identities or personality states. Each identity exhibits unique patterns of behavior, voice, and mannerisms and may possess separate memories and emotional responses. The alternating control between identities can result in memory gaps and challenges in recalling daily activities, often exacerbating the individual's...
Type II Diabetes I: Introduction01:26

Type II Diabetes I: Introduction

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
Cerebrum: Anatomical Overview II01:11

Cerebrum: Anatomical Overview II

Each cerebral hemisphere can be divided into three main regions. The outermost region, the cerebral cortex, is a thin layer (2 to 4 millimeters thick) made up of gray matter, consisting of neuron cell bodies, dendrites, glial cells, and blood vessels. The middle region, or white matter, is primarily composed of myelinated nerve fibers organized into three types of large tracts: association fibers, commissures, and projection fibers. Association fibers connect different areas within the same...
Cushing Syndrome II: Pathophysiology01:19

Cushing Syndrome II: Pathophysiology

Cortisol production is normally governed by the hypothalamic–pituitary–adrenal (HPA) axis, which maintains hormonal balance through tightly regulated feedback mechanisms. Disruption of this regulatory system is central to the development of Cushing syndrome, whether the excess cortisol originates from external medications or internal pathology. Persistent cortisol elevation alters metabolism, immune function, and endocrine signaling, producing the characteristic clinical features of the...