Lesions of the parietal lobe, which often result from stroke or neoplasms, tend to involve superior fibers first, causing contralateral inferior homonymous hemianopic defects. More extensive lesions involve the superior visual fields but remain denser inferiorly. Parietal lobe syndromes encompass a wide variety of other neurologic effects, including perceptual problems (agnosia) and apraxia. Lesions of the dominant parietal lobe cause Gerstmann syndrome, a combination of acalculia, agraphia, finger agnosia, and left–right confusion. Lesions in the nondominant parietal lobe can cause contralateral neglect (see Chapter 6).
Damage to pursuit pathways that converge in the posterior parietal lobes (near the visual radiations) may cause abnormalities in optokinetic nystagmus (OKN). The examiner elicits the impaired OKN response by moving targets toward the lesion, inducing attempts to use the damaged pursuit pathway. Thus, a patient with a homonymous hemianopia due to a parietal lobe lesion will have a reduced OKN response with the target moving toward the affected side, whereas a patient with a homonymous hemianopia due to a lesion of the optic tract or occipital lobe will have an intact OKN response (see Chapter 8).
Excerpted from BCSC 2020-2021 series: Section 5 - Neuro-Ophthalmology. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.