Description of brain injury in the amnesic patient N.A. Based on magnetic resonance imaging

Larry R. Squire, David G Amaral, Stuart Zola-Morgan, Mark Kritchevsky, Gary Press

Research output: Contribution to journalArticle

91 Citations (Scopus)

Abstract

N.A. has been amnesic since 1960 when at the age of 22 years he sustained a penetrating brain injury with a miniature fencing foil. The amnesia primarily affects verbal material and occurs in the absence of other detectable cognitive deficits. Previous CT scans demonstrated a lucency in the region of the left mediodorsal thalamic nucleus, but no additional damage was revealed. Beginning in 1986 when he was 48 years old, N.A. was evaluated with a series of magnetic resonance imaging (MR) studies. Three major areas of damage were identified. In the left thalamus there is a prominent 3- to 4-mm-wide linear lesion that approximates the position and orientation of the internal medullary lamina. The defect extends for approximately 20 mm anteroposteriorly and likely involves the rostral group of intralaminar nuclei (central medial, paracentral, central lateral, rhomboid, and reuniens nuclei), the caudal group of intralaminar nuclei (centrum medianum and parafascicular nuclei), the ventral aspects of the mediodorsal nucleus, and the ventral lateral and ventral anterior nuclei. It also likely interrupts the trajectories of the mammillothalamic tract and postcommissural fornix. The posterior hypothalamus is markedly disrupted and the mammillary nuclei appear to be missing bilaterally. Finally, the right anterior temporal lobe is damaged for a distance of about 3.5 cm from the pole to midway through the amygdaloid complex. This damage probably occurred during exploratory neurosurgery done at the time of N.A.'s injury. The hippocampal formation appears intact on both sides. A comparison of these findings with those from other patients with diencephalic amnesia suggests that amnesia can result when several diencephalic structures are damaged conjointly, including the internal medullary lamina, the intralaminar nuclei, the mediodorsal nucleus, and the mammillothalamic tract. Whether amnesia as severe as N.A.'s would result from selective damage to any one of these structures remains to be determined.

Original languageEnglish (US)
Pages (from-to)23-35
Number of pages13
JournalExperimental Neurology
Volume105
Issue number1
DOIs
StatePublished - 1989

Fingerprint

Intralaminar Thalamic Nuclei
Amnesia
Mediodorsal Thalamic Nucleus
Brain Injuries
Midline Thalamic Nuclei
Magnetic Resonance Imaging
Penetrating Head Injuries
Posterior Hypothalamus
Ventral Thalamic Nuclei
Neurosurgery
Temporal Lobe
Thalamus
Hippocampus
Wounds and Injuries

ASJC Scopus subject areas

  • Neuroscience(all)
  • Neurology

Cite this

Description of brain injury in the amnesic patient N.A. Based on magnetic resonance imaging. / Squire, Larry R.; Amaral, David G; Zola-Morgan, Stuart; Kritchevsky, Mark; Press, Gary.

In: Experimental Neurology, Vol. 105, No. 1, 1989, p. 23-35.

Research output: Contribution to journalArticle

Squire, Larry R. ; Amaral, David G ; Zola-Morgan, Stuart ; Kritchevsky, Mark ; Press, Gary. / Description of brain injury in the amnesic patient N.A. Based on magnetic resonance imaging. In: Experimental Neurology. 1989 ; Vol. 105, No. 1. pp. 23-35.
@article{5eb3c553ef5948aa8c5225153b1cef8e,
title = "Description of brain injury in the amnesic patient N.A. Based on magnetic resonance imaging",
abstract = "N.A. has been amnesic since 1960 when at the age of 22 years he sustained a penetrating brain injury with a miniature fencing foil. The amnesia primarily affects verbal material and occurs in the absence of other detectable cognitive deficits. Previous CT scans demonstrated a lucency in the region of the left mediodorsal thalamic nucleus, but no additional damage was revealed. Beginning in 1986 when he was 48 years old, N.A. was evaluated with a series of magnetic resonance imaging (MR) studies. Three major areas of damage were identified. In the left thalamus there is a prominent 3- to 4-mm-wide linear lesion that approximates the position and orientation of the internal medullary lamina. The defect extends for approximately 20 mm anteroposteriorly and likely involves the rostral group of intralaminar nuclei (central medial, paracentral, central lateral, rhomboid, and reuniens nuclei), the caudal group of intralaminar nuclei (centrum medianum and parafascicular nuclei), the ventral aspects of the mediodorsal nucleus, and the ventral lateral and ventral anterior nuclei. It also likely interrupts the trajectories of the mammillothalamic tract and postcommissural fornix. The posterior hypothalamus is markedly disrupted and the mammillary nuclei appear to be missing bilaterally. Finally, the right anterior temporal lobe is damaged for a distance of about 3.5 cm from the pole to midway through the amygdaloid complex. This damage probably occurred during exploratory neurosurgery done at the time of N.A.'s injury. The hippocampal formation appears intact on both sides. A comparison of these findings with those from other patients with diencephalic amnesia suggests that amnesia can result when several diencephalic structures are damaged conjointly, including the internal medullary lamina, the intralaminar nuclei, the mediodorsal nucleus, and the mammillothalamic tract. Whether amnesia as severe as N.A.'s would result from selective damage to any one of these structures remains to be determined.",
author = "Squire, {Larry R.} and Amaral, {David G} and Stuart Zola-Morgan and Mark Kritchevsky and Gary Press",
year = "1989",
doi = "10.1016/0014-4886(89)90168-4",
language = "English (US)",
volume = "105",
pages = "23--35",
journal = "Experimental Neurology",
issn = "0014-4886",
publisher = "Academic Press Inc.",
number = "1",

}

TY - JOUR

T1 - Description of brain injury in the amnesic patient N.A. Based on magnetic resonance imaging

AU - Squire, Larry R.

AU - Amaral, David G

AU - Zola-Morgan, Stuart

AU - Kritchevsky, Mark

AU - Press, Gary

PY - 1989

Y1 - 1989

N2 - N.A. has been amnesic since 1960 when at the age of 22 years he sustained a penetrating brain injury with a miniature fencing foil. The amnesia primarily affects verbal material and occurs in the absence of other detectable cognitive deficits. Previous CT scans demonstrated a lucency in the region of the left mediodorsal thalamic nucleus, but no additional damage was revealed. Beginning in 1986 when he was 48 years old, N.A. was evaluated with a series of magnetic resonance imaging (MR) studies. Three major areas of damage were identified. In the left thalamus there is a prominent 3- to 4-mm-wide linear lesion that approximates the position and orientation of the internal medullary lamina. The defect extends for approximately 20 mm anteroposteriorly and likely involves the rostral group of intralaminar nuclei (central medial, paracentral, central lateral, rhomboid, and reuniens nuclei), the caudal group of intralaminar nuclei (centrum medianum and parafascicular nuclei), the ventral aspects of the mediodorsal nucleus, and the ventral lateral and ventral anterior nuclei. It also likely interrupts the trajectories of the mammillothalamic tract and postcommissural fornix. The posterior hypothalamus is markedly disrupted and the mammillary nuclei appear to be missing bilaterally. Finally, the right anterior temporal lobe is damaged for a distance of about 3.5 cm from the pole to midway through the amygdaloid complex. This damage probably occurred during exploratory neurosurgery done at the time of N.A.'s injury. The hippocampal formation appears intact on both sides. A comparison of these findings with those from other patients with diencephalic amnesia suggests that amnesia can result when several diencephalic structures are damaged conjointly, including the internal medullary lamina, the intralaminar nuclei, the mediodorsal nucleus, and the mammillothalamic tract. Whether amnesia as severe as N.A.'s would result from selective damage to any one of these structures remains to be determined.

AB - N.A. has been amnesic since 1960 when at the age of 22 years he sustained a penetrating brain injury with a miniature fencing foil. The amnesia primarily affects verbal material and occurs in the absence of other detectable cognitive deficits. Previous CT scans demonstrated a lucency in the region of the left mediodorsal thalamic nucleus, but no additional damage was revealed. Beginning in 1986 when he was 48 years old, N.A. was evaluated with a series of magnetic resonance imaging (MR) studies. Three major areas of damage were identified. In the left thalamus there is a prominent 3- to 4-mm-wide linear lesion that approximates the position and orientation of the internal medullary lamina. The defect extends for approximately 20 mm anteroposteriorly and likely involves the rostral group of intralaminar nuclei (central medial, paracentral, central lateral, rhomboid, and reuniens nuclei), the caudal group of intralaminar nuclei (centrum medianum and parafascicular nuclei), the ventral aspects of the mediodorsal nucleus, and the ventral lateral and ventral anterior nuclei. It also likely interrupts the trajectories of the mammillothalamic tract and postcommissural fornix. The posterior hypothalamus is markedly disrupted and the mammillary nuclei appear to be missing bilaterally. Finally, the right anterior temporal lobe is damaged for a distance of about 3.5 cm from the pole to midway through the amygdaloid complex. This damage probably occurred during exploratory neurosurgery done at the time of N.A.'s injury. The hippocampal formation appears intact on both sides. A comparison of these findings with those from other patients with diencephalic amnesia suggests that amnesia can result when several diencephalic structures are damaged conjointly, including the internal medullary lamina, the intralaminar nuclei, the mediodorsal nucleus, and the mammillothalamic tract. Whether amnesia as severe as N.A.'s would result from selective damage to any one of these structures remains to be determined.

UR - http://www.scopus.com/inward/record.url?scp=0024319147&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024319147&partnerID=8YFLogxK

U2 - 10.1016/0014-4886(89)90168-4

DO - 10.1016/0014-4886(89)90168-4

M3 - Article

C2 - 2744126

AN - SCOPUS:0024319147

VL - 105

SP - 23

EP - 35

JO - Experimental Neurology

JF - Experimental Neurology

SN - 0014-4886

IS - 1

ER -