Parietal lobe

Parietal lobe
Principal fissures and lobes of the cerebrum viewed laterally. (Parietal lobe is shown in yellow)
Lateral surface of left cerebral hemisphere, viewed from the side. (Parietal lobe is shown in orange.)
Details
Pronunciation/pəˈr.ɪtəl/ pə-RY-it-əl[1]
Part ofCerebrum
ArteryAnterior cerebral
Middle cerebral
VeinSuperior sagittal sinus
Identifiers
Latinlobus parietalis
MeSHD010296
NeuroNames95
NeuroLex IDbirnlex_1148
TA98A14.1.09.123
TA25467
FMA61826
Anatomical terms of neuroanatomy

The parietal lobe is one of the four major lobes of the cerebral cortex in the brain of mammals. The parietal lobe is positioned above the temporal lobe and behind the frontal lobe and central sulcus.

The parietal lobe integrates sensory information among various modalities, including spatial sense and navigation (proprioception), the main sensory receptive area for the sense of touch in the somatosensory cortex which is just posterior to the central sulcus in the postcentral gyrus,[2] and the dorsal stream of the visual system. The major sensory inputs from the skin (touch, temperature, and pain receptors), relay through the thalamus to the parietal lobe.

Several areas of the parietal lobe are important in language processing. The somatosensory cortex can be illustrated as a distorted figure – the cortical homunculus[3] (Latin: "little man") in which the body parts are rendered according to how much of the somatosensory cortex is devoted to them.[4] The superior parietal lobule and inferior parietal lobule are the primary areas of body or spatial awareness. A lesion commonly in the right superior or inferior parietal lobule leads to hemispatial neglect.

The name comes from the parietal bone, which is named from the Latin paries-, meaning "wall".

Structure

Animation. Parietal lobe (red) of left cerebral hemisphere.

The parietal lobe is defined by three anatomical boundaries: The central sulcus separates the parietal lobe from the frontal lobe; the parieto-occipital sulcus separates the parietal and occipital lobes; the lateral sulcus (sylvian fissure) is the most lateral boundary, separating it from the temporal lobe; and the longitudinal fissure divides the two hemispheres. Within each hemisphere, the somatosensory cortex represents the skin area on the contralateral surface of the body.[4]

Immediately posterior to the central sulcus, and the most anterior part of the parietal lobe, is the postcentral gyrus (Brodmann area 3), the primary somatosensory cortical area. Separating this from the posterior parietal cortex is the postcentral sulcus.

The posterior parietal cortex can be subdivided into the superior parietal lobule (Brodmann areas 5 + 7) and the inferior parietal lobule (39 + 40), separated by the intraparietal sulcus (IPS). The intraparietal sulcus and adjacent gyri are essential in guidance of limb and eye movement, and—based on cytoarchitectural and functional differences—is further divided into medial (MIP), lateral (LIP), ventral (VIP), and anterior (AIP) areas.

Function

Functions of the parietal lobe include:

  • Two point discrimination – through touch alone without other sensory input (e.g. visual)
  • Graphesthesia – recognizing writing on skin by touch alone
  • Touch localization (bilateral simultaneous stimulation)

The parietal lobe plays important roles in integrating sensory information from various parts of the body, knowledge of numbers and their relations,[5] and in the manipulation of objects. Its function also includes processing information relating to the sense of touch.[6] Portions of the parietal lobe are involved with visuospatial processing.[7] Although multisensory in nature, the posterior parietal cortex is often referred to by vision scientists as the dorsal stream of vision (as opposed to the ventral stream in the temporal lobe). This dorsal stream has been called both the "where" stream (as in spatial vision)[8] and the "how" stream (as in vision for action).[9] The posterior parietal cortex (PPC) receives somatosensory and visual input, which then, through motor signals, controls movement of the arm, hand, and eyes.[10]

Various studies in the 1990s found that different regions of the posterior parietal cortex in macaques represent different parts of space.

  • The lateral intraparietal (LIP) area contains a map of neurons (retinotopically-coded when the eyes are fixed[11]) representing the saliency of spatial locations, and attention to these spatial locations. It can be used by the oculomotor system for targeting eye movements, when appropriate.[12]
  • The ventral intraparietal (VIP) area receives input from a number of senses (visual, somatosensory, auditory, and vestibular[13]). Neurons with tactile receptive fields represent space in a head-centered reference frame.[13] The cells with visual receptive fields also fire with head-centered reference frames[14] but possibly also with eye-centered coordinates[13]
  • The medial intraparietal (MIP) area neurons encode the location of a reach target in eye-centered coordinates.[15]
  • The anterior intraparietal (AIP) area contains neurons responsive to shape, size, and orientation of objects to be grasped[16] as well as for manipulation of the hands themselves, both to viewed[16] and remembered stimuli.[17] The AIP has neurons that are responsible for grasping and manipulating objects through motor and visual inputs. The AIP and ventral premotor together are responsible for visuomotor transformations for actions of the hand.[10]

More recent fMRI studies have shown that humans have similar functional regions in and around the intraparietal sulcus and parietal-occipital junction.[18] The human "parietal eye fields" and "parietal reach region", equivalent to LIP and MIP in the monkey, also appear to be organized in gaze-centered coordinates so that their goal-related activity is "remapped" when the eyes move.[19]

Emerging evidence has linked processing in the inferior parietal lobe to declarative memory. Bilateral damage to this brain region does not cause amnesia however the strength of memory is diminished, details of complex events become harder to retrieve, and subjective confidence in memory is very low.[20][21][22] This has been interpreted as reflecting either deficits in internal attention,[23] deficits in subjective memory states,[22] or problems with the computation that allows evidence to accumulate, thus allowing decisions to be made about internal representations.[20]

Clinical significance

Features of parietal lobe lesions are as follows:

  • Unilateral parietal lobe
    • Contralateral hemisensory loss
    • Astereognosis – inability to determine 3-D shape by touch.
    • Agraphaesthesia – inability to read numbers or letters drawn on hand, with eyes shut.
    • Contralateral homonymous inferior quadrantanopia
    • Asymmetry of optokinetic nystagmus (OKN)
    • Sensory seizures
  • Dominant hemisphere
    • Conduction aphasia
    • Dyslexia – a general term for disorders that can involve difficulty in learning to read or interpret words, letters, and other symbols
    • Apraxia – inability to perform complex movements in the presence of normal motor, sensory and cerebellar function
    • Gerstmann syndrome – characterized by acalculia, agraphia, finger agnosia, and left-right disorientation
  • Non-dominant hemisphere
  • Bilateral hemispheres

Damage to this lobe in the right hemisphere results in the loss of imagery, visualization of spatial relationships and neglect of left-side space and left side of the body. Even drawings may be neglected on the left side. Damage to this lobe in the left hemisphere will result in problems in mathematics, long reading, writing, and understanding symbols. The parietal association cortex enables individuals to read, write, and solve mathematical problems. The sensory inputs from the right side of the body go to the left side of the brain and vice versa.

The syndrome of hemispatial neglect is usually associated with large deficits of attention of the non-dominant hemisphere. Optic ataxia is associated with difficulties reaching toward objects in the visual field opposite to the side of the parietal damage. Some aspects of optic ataxia have been explained in terms of the functional organization described above.

Apraxia is a disorder of motor control which can be referred neither to "elemental" motor deficits nor to general cognitive impairment. The concept of apraxia was shaped by Hugo Liepmann.[24][25] Apraxia is predominantly a symptom of left brain damage, but some symptoms of apraxia can also occur after right brain damage.[26]

Amorphosynthesis is a loss of perception on one side of the body caused by a lesion in the parietal lobe. Usually, left-sided lesions cause agnosia, a full-body loss of perception, while right-sided lesions cause lack of recognition of the person's left side and extrapersonal space. The term amorphosynthesis was coined by D. Denny-Brown to describe patients he studied in the 1950s.[27]

Can also result in sensory impairment where one of the affected person's senses (sight, hearing, smell, touch, taste and spatial awareness) is no longer normal.[clarification needed][28][29]

See also

References

  1. ^ "PARIETAL | meaning in the Cambridge English Dictionary".
  2. ^ "Parietal Lobe".
  3. ^ The cortical homunculus should not be confused with the more general homunculus concept for a "spectator within the brain"; see work by psychologist David Marr for more information on this.
  4. ^ a b Schacter DL, Gilbert DL, Wegner DM (2009). Psychology (2nd ed.). New York (NY): Worth Publishers.
  5. ^ Blakemore SJ, Firth U (2005). The learning brain: lessons for education. Malden, MA, USA: Blackwell. ISBN 978-1-4051-2401-0.
  6. ^ Penfield W, Rasmussen T (1950). The cerebral cortex of a man: A clinical study of localization of function. New York: Macmillan.
  7. ^ Baldauf D, Cui H, Andersen RA (October 2008). "The posterior parietal cortex encodes in parallel both goals for double-reach sequences". The Journal of Neuroscience. 28 (40): 10081–9. doi:10.1523/JNEUROSCI.3423-08.2008. PMC 2744218. PMID 18829966.
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  11. ^ Kusunoki M, Goldberg ME (March 2003). "The time course of perisaccadic receptive field shifts in the lateral intraparietal area of the monkey". Journal of Neurophysiology. 89 (3): 1519–27. CiteSeerX 10.1.1.580.120. doi:10.1152/jn.00519.2002. PMID 12612015.
  12. ^ Goldberg ME, Bisley JW, Powell KD, Gottlieb J (2006). "Chapter 10 Saccades, salience and attention: The role of the lateral intraparietal area in visual behavior". Visual Perception - Fundamentals of Awareness: Multi-Sensory Integration and High-Order Perception. Progress in Brain Research. Vol. 155. pp. 157–75. doi:10.1016/S0079-6123(06)55010-1. ISBN 9780444519276. PMC 3615538. PMID 17027387. {{cite book}}: |journal= ignored (help)
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  14. ^ Zhang T, Heuer HW, Britten KH (June 2004). "Parietal area VIP neuronal responses to heading stimuli are encoded in head-centered coordinates". Neuron. 42 (6): 993–1001. doi:10.1016/j.neuron.2004.06.008. PMID 15207243.
  15. ^ Pesaran B, Nelson MJ, Andersen RA (July 2006). "Dorsal premotor neurons encode the relative position of the hand, eye, and goal during reach planning". Neuron. 51 (1): 125–34. doi:10.1016/j.neuron.2006.05.025. PMC 3066049. PMID 16815337.
  16. ^ a b Murata A, Gallese V, Luppino G, Kaseda M, Sakata H (May 2000). "Selectivity for the shape, size, and orientation of objects for grasping in neurons of monkey parietal area AIP". Journal of Neurophysiology. 83 (5): 2580–601. doi:10.1152/jn.2000.83.5.2580. PMID 10805659. S2CID 15140300.
  17. ^ Murata A, Gallese V, Kaseda M, Sakata H (May 1996). "Parietal neurons related to memory-guided hand manipulation". Journal of Neurophysiology. 75 (5): 2180–6. doi:10.1152/jn.1996.75.5.2180. PMID 8734616.
  18. ^ Culham JC, Valyear KF (April 2006). "Human parietal cortex in action". Current Opinion in Neurobiology. 16 (2): 205–12. doi:10.1016/j.conb.2006.03.005. PMID 16563735. S2CID 18561181.
  19. ^ Medendorp WP, Goltz HC, Vilis T, Crawford JD (July 2003). "Gaze-centered updating of visual space in human parietal cortex". The Journal of Neuroscience. 23 (15): 6209–14. doi:10.1523/JNEUROSCI.23-15-06209.2003. PMC 6740538. PMID 12867504.
  20. ^ a b Dobbins IG, Jaeger A, Studer B, Simons JS (November 2012). "Use of explicit memory cues following parietal lobe lesions". Neuropsychologia. 50 (13): 2992–3003. doi:10.1016/j.neuropsychologia.2012.07.037. PMC 3595063. PMID 22975148.
  21. ^ Berryhill ME, Phuong L, Picasso L, Cabeza R, Olson IR (December 2007). "Parietal lobe and episodic memory: bilateral damage causes impaired free recall of autobiographical memory". The Journal of Neuroscience. 27 (52): 14415–23. doi:10.1523/JNEUROSCI.4163-07.2007. PMC 6673454. PMID 18160649.
  22. ^ a b Hower KH, Wixted J, Berryhill ME, Olson IR (April 2014). "Impaired perception of mnemonic oldness, but not mnemonic newness, after parietal lobe damage". Neuropsychologia. 56: 409–17. doi:10.1016/j.neuropsychologia.2014.02.014. PMC 4075961. PMID 24565734.
  23. ^ Cabeza R, Ciaramelli E, Olson IR, Moscovitch M (August 2008). "The parietal cortex and episodic memory: an attentional account". Nature Reviews. Neuroscience. 9 (8): 613–25. doi:10.1038/nrn2459. PMC 2692883. PMID 18641668.
  24. ^ Goldenberg G (May 2009). "Apraxia and the parietal lobes". Neuropsychologia. 47 (6): 1449–59. doi:10.1016/j.neuropsychologia.2008.07.014. PMID 18692079. S2CID 41741275.
  25. ^ Liepmann, 1900 [clarification needed]
  26. ^ Khan AZ, Pisella L, Vighetto A, Cotton F, Luauté J, Boisson D, et al. (April 2005). "Optic ataxia errors depend on remapped, not viewed, target location". Nature Neuroscience. 8 (4): 418–20. doi:10.1038/nn1425. PMID 15768034. S2CID 24813342.
  27. ^ Denny-Brown D, Banker BQ (March 1954). "Amorphosynthesis from left parietal lesion". A.M.A. Archives of Neurology and Psychiatry. 71 (3): 302–13. doi:10.1001/archneurpsyc.1954.02320390032003. PMID 13123592.
  28. ^ Rahal S (28 November 2019). "How the Symptoms of Alzheimer's are Related to the Brain Lobe Affected". verywell.health. Archived from the original on 19 November 2012. Retrieved 4 December 2012.
  29. ^ Yildiz M, Borgwardt SJ, Berger GE (2011). "Parietal lobes in schizophrenia: do they matter?". Schizophrenia Research and Treatment. 2011: 581686. doi:10.1155/2011/581686. PMC 3420742. PMID 22937268.

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