Corpora amylacea: a marker for mesial temporal sclerosis

M H Chung1, D S Horoupian

  • 1Division of Neuropathology, Stanford University Medical Center, California 94305-5324, USA.

Insights

Corpora amylacea (CoA) are frequently found with mesial temporal sclerosis (MTS), a common cause of intractable epilepsy. Abundant CoA can serve as a diagnostic marker for MTS when neuronal loss is unclear.

Area of Science:

  • Neuropathology
  • Epilepsy Research
  • Histopathology

Background:

  • Mesial temporal sclerosis (MTS) is the primary pathology in temporal lobectomies for intractable seizures.
  • Diagnosing MTS relies on identifying hippocampal neuronal loss, which can be challenging in non-en bloc resections.
  • Indeterminate hippocampal pathology is a common issue in epilepsy surgery evaluations.

Purpose of the Study:

  • To investigate the association between corpora amylacea (CoA) and mesial temporal sclerosis (MTS).
  • To evaluate the utility of CoA as a diagnostic marker for MTS in epilepsy surgery specimens.
  • To recommend optimal staining techniques for identifying CoA in resected temporal lobe tissues.

Main Methods:

  • Retrospective analysis of 73 temporal lobectomies performed for seizure disorders.
  • Histopathological examination of hippocampal and amygdala tissues.
  • Staining with LFB-PAS to highlight corpora amylacea (CoA).

Main Results:

  • Increased numbers of corpora amylacea (CoA) were observed in 58% of cases with mesial temporal sclerosis (MTS).
  • Corpora amylacea (CoA) presence was associated with MTS, offering a potential diagnostic marker.
  • The identification of abundant CoA can aid diagnosis when neuronal loss is difficult to assess.

Conclusions:

  • Corpora amylacea (CoA) are frequently associated with mesial temporal sclerosis (MTS).
  • Abundant CoA serves as a valuable histological marker for MTS, especially when neuronal loss is equivocal.
  • LFB-PAS staining of hippocampal and amygdala tissues is recommended for highlighting CoA in temporal lobe epilepsy evaluations.

Related Concept Videos

Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...
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...
Dementia l: Introduction01:22

Dementia l: Introduction

Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...