Spatial Awareness—A Function of the Temporal Lobe
Abstract & Commentary
Source: Karnath HO, Ferber S, Himmelbach M. Nature. 2001;411:950-953.
Acute hemi-spatial unawareness in humans, sometimes called "neglect," has long been considered to be the result of acute, severe damage to the right posterior-inferior parietal lobe. Infarcts, hemorrhages, or occasionally, neoplasms, may precipitate such injuries and the functional deficit often fails to recover completely. In some instances, the affected patient cannot recognize the left side of his body or outer space. Indeed, he even may deny the existence of the left half of his own self. Such abrupt, total losses of seemingly instinctive knowledge can appropriately be considered as focal unconsciousness. This clinical report has concentrated on primary damage to the right inferior parietal lobule (IPL), the temporo-parieto-occiptal (TPO) junction, and the superior temporal gyrus (STG).The primary cortical visual system has been avoided but the precortical TPO pathway frequently interrupts parts or all of the subsequent TPO injury.
Karnath and associates, over a 5-year period, have quantified and qualified the correctness of a new concept. They emphasize that most or all past clinical reports or discussions of spatial neglect have focused on parietal lobe dysfunction. Meanwhile, most reports have ignored the concurrent injuries that affected the adjacent geniculo-occipital pathways of the cerebral visual system. Recognizing this potential confusion of 2 dysfunctional perceptive systems, Karnath et al used quantitative CT or MRI scanning measures to identify cerebral functions in 49 patients who suffered from only purely’ left spatial unawareness. (This indicated that no patient displayed any specific visual dysfunction.) Of the initial 49 patients, 33 had cortical lesions and the remainder suffered only subcortical abnormalities that unclearly engendered spatial unawareness. Eight of the subcortical group also had unrelated cortical abnormalities and was put aside. This left 25 uncomplicated patients. Each of the 25 patients underwent a careful neurological examination plus pre-programmed CT or MRI brain imaging. Each instrument was preadjusted to provide 8 designated horizontal slices of functional interest.
Imaging results of each of the 25 clinically dysfunctional patients were anatomically and quantitatively similar to the expected changes in every case. Karnath et al state, "In clear contrast to controls, the lesion overlap in the neglect patients centered on the (right) STG (Brodmann areas 22 and 42). Neighboring affected structures consisted of the ventral postcentral gyrus and the operculum." The STG damage amounted to 6.9 times larger in size in neglect patients than at normal baseline (P < 0.001). No other predominant involvement in size occurred in the IPL, TPO, the cingulate cortex, or the middle temporal gyrus in patients with pure spatial neglect. Less intense injury affected the ventral post central gyrus and the operculum which functionally joins together the parietal, occipital, and temporal lobes. Unexpectedly, these "pure" patients who lacked visual defects expressed little or no functional involvement that affected the inferior parietal lobule, the temporal-parietal-occipital junction, the cingulate cortex, or the middle temporal gyrus. Furthermore, Karnath et al cite an additional 25 paired patients who suffered cerebral injury in the frontal-parietal areas but spared the STG and avoided any clinical neglect.
Past clinical opinion has often considered that an injured parietal area singularly generated agnosia when compounded with an ipsilateral visual abnormality. Karnath et al of this present report, however, suggest a more likely interpretation of such double-system dysfunctions. To resolve this question, Karnath et al studied 8 patients with acute right-hemispheric strokes. Four of these suffered neglect associated with severe vascular damage to the right parietal lobe plus concurrent injury to the optic radiation as it passes from the posterior horn of the lateral ventricle to reach the occipital cortex. It invoked high dysfunction in the IPL, the TPO junction, and the STG.
Karnath et al conclude that 4 patterns of damage can construct neglect: "1) A clear difference in lesion location between patients with pure neglect and those with both neglect and hemianopia (the latter involving also posterior regions); 2) those areas found as the neural correlate of spatial neglect in patients with pure neglect are affected in the patients suffering from both neglect and hemianopia; 3) the center of lesion overlap in patients with neglect and hemianopia is comparable to that reported in earlier studies (that is, involves the IPL and TPO junction); and 4) the posterior parts of lesion overlap in the patients with neglect and hemianopia also overlap in those patients without neglect but with hemianopia due to a stroke in the territory of the same cerebral artery."
Commentary
In monkeys, damage to STG alone fails to impair accurate, bilateral recognition of spatial objects. Spatial knowledge provides these animals with their very survival. Unlike mankind, however, their small abstract verbal signals prevent intellectual complexity. So-called spatial or object neglect in humans is much more than that. It’s focal unconsciousness, known by the quaint early 20th century term of agnosia. Your editor should have recognized a long time ago that a sudden unknown loss of spatial memory cannot by itself be engendered by an injury confined to the parietal lobe. Nor does selective V1-3 damage induce upon persons a state of permanent, unconscious hemianopsia. Temporal lobe damage is required to completely invoke that disability, just as it must do in sustained human spatial unconsciousness. —Fred Plum
Plum, MD, University Professor, Weill Medical College, and Attending Neurologist, NY Presbyterian Hospital, is Editor of Neurology Alert.
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