Parietal lobe

From Wikipedia, the free encyclopedia
Jump to: navigation, search
Brain: Parietal lobe

Principal fissures and lobes of the cerebrum viewed laterally. (Parietal lobe is shown in yellow)
Gray726 parietal lobe.png
Lateral surface of left cerebral hemisphere, viewed from the side. (Parietal lobe is shown in orange.)
Latin lobus parietalis
Gray's p.822
Part of Cerebrum
Anterior cerebral
Middle cerebral
Superior sagittal sinus
NeuroNames hier-77
MeSH Parietal+Lobe
NeuroLex ID birnlex_1148
TA A14.1.09.123
FMA FMA:61826

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 (superior to) the occipital lobe and behind (posterior to) the frontal lobe and central sulcus.

The parietal lobe integrates sensory information among various modalities, including spatial sense and navigation (See proprioception), the main sensory receptive area for the sense of touch (See somatosensation) in the somatosensory cortex which is just posterior to the central sulcus in the postcentral gyrus,[1] 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 parietal lobe.

Several portions of the parietal lobe are important in language processing. The somatosensory cortex can be illustrated as a distorted figure — the homunculus (Latin: "little man"), in which the body parts are rendered according to how much of the somatosensory cortex is devoted to them.[2] The superior parietal lobule and inferior parietal lobule are the primary areas of body or spatial awareness. A lesion in the superior or inferior parietal lobule leads to hemineglect.

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


Animation. Parietal lobe (red) of leftcerebral hemisphere.

The parietal lobe is defined by three anafissure divides the two hemispheres. Within each hemisphere, the somatosensory cortex represents the skin area on the contralateral surface of the body.[2]

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. Dividing this and 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.

Clinical significance[edit]

Damage to the right hemisphere of this lobe 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 the left hemisphere of this lobe 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.

Gerstmann's syndrome is associated with lesion to the dominant (usually left) parietal lobe.[3] Balint's syndrome is associated with bilateral lesions. 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 about a hundred years ago.[4][5] Apraxia is predominantly a symptom of left brain damage, but some symptoms of apraxia can also occur after right brain damage.[6]

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.[7]

Can also result in sensory impairment when one of your senses (sight, hearing, smell, touch, taste and spatial awareness) is no longer normal.[8]

Several studies have suggested that abnormal parietal function may be associated with schizophrenia. There is a possibility that grey matter abnormalities begin in parietal and occipital lobes, progress towards the frontal regions, causing schizophrenia structural and functional alterations.[9]

Additional images[edit]

See also[edit]


  1. ^[full citation needed]
  2. ^ a b Schacter, D. L., Gilbert, D. L. & Wegner, D. M. (2009). Psychology. (2nd ed.). New Work (NY): Worth Publishers.[page needed]
  3. ^ Vallar G (July 2007). "Spatial neglect, Balint-Homes' and Gerstmann's syndrome, and other spatial disorders". CNS Spectrums 12 (7): 527–36. PMID 17603404. 
  4. ^ Goldenberg G (May 2009). "Apraxia and the parietal lobes". Neuropsychologia 47 (6): 1449–59. doi:10.1016/j.neuropsychologia.2008.07.014. PMID 18692079. 
  5. ^ Liepmann, 1900[clarification needed]
  6. ^ Khan AZ, Pisella L, Vighetto A, 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. 
  7. ^ Denny-Brown D, Banker BQ (March 1954). "Amorphosynthesis from left parietal lesion". Archives of Neurology and Psychiatry 71 (3): 302–13. doi:10.1001/archneurpsyc.1954.02320390032003. PMID 13123592. 
  8. ^[full citation needed]
  9. ^ 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.