Associated Neurological Findings

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Cerebral. Hemianopias that result from lesions of the optic radiations are often associated with other "cortically-based" neurological findings. Temporal lobe lesions may be accompanied by personality changes, complex partial seizures, memory deficits, fluent aphasia (if the dominant side is involved), or Kluver-Bucy syndrome (hypersexuality, placidity, hyperorality, visual and auditory agnosia, and apathy) with involvement of the anterior temporal lobes bilaterally. Conduction aphasia, Gerstmann's syndrome (finger agnosia, agraphia, acalculia, and right-left disorientation), and tactile agnosia, all suggest a dominant parietal lobe process. Left-sided neglect, topographic memory loss, constructional and dressing apraxias, in asssociation with a left hemianopia, suggest a nondominant parietal lesion. More parieto-occipital or occipitally-based visual disturbances such as in Balint's syndrome or cortical blindness may accompany dementia in Creutzfeldt-Jakob disease, progressive multifocal leukoencephalopathy, or Alzheimer's disease.

Cranial Nerves. Lesions causing visual loss and ocular motility deficits frequently exhibit characteristic recognizable iii symptom complexes. For instance, orbital apex disturbances cause an optic neuropathy and third, fourth, and sixth cranial nerve dysfunction, as well as cranial nerve V1 distribution sensory loss, and oculosympathetic paresis. Suprasellar masses may compress the optic chiasm, and if large enough, can extend laterally to involve cranial nerves III, IV, Vi, V1, and V2 within the cavernous sinus. In rare instances, seesaw nystagmus occurs in association with sellar lesions with bitemporal hemianopias. In this unique motility disturbance, one eye elevates and intorts while the other depresses and extorts, then the process reverses and repeats. Deep parietal lobe lesions can produce a homonymous hemianopia and poor tracking of objects moving toward the lesion. This effect results from involvement of the optic radiations and adjacent descending corticobulbar fibers from the parieto-occipitotemporal pursuit area.

In contrast, normal optokinetic responses can be expected in a hemianopia due to a lesion solely within the occipital lobe. Bilateral parietal lesions may cause abnormal initiation of voluntary eye movements, despite normal reflex saccades and pursuit (ocular motor apraxia), as seen in Balint's syndrome (see later). Hemianopias related to occipital lobe infarction may be associated with brain stem ocular motor dysfunction, if the etiology is vertebrobasilar occlusion. Patients with a hemianopia or neglect may have a gaze preference away from the visual deficit.

Patients with cerebellar disease and acquired nystagmus, particularly pendular, may complain of oscillopsia, the illusion of motion, and may suffer a reduction in visual acuity. Conversely, patients with bilateral visual loss involving the anterior visual pathways, especially if congenital or acquired in childhood, may develop nystagmus with vertical and horizontal components.^ Patients with severe visual loss of any type may also display a "searching" nystagmus in their attempt to localize objects without adequate visual feedback.

Patients with multiple sclerosis presenting with optic neuritis may have nystagmus or a unilateral or bilateral internuclear ophthalmoplegia, indicating previous white matter involvement in the posterior fossa.

Motor/Reflexes/Cerebellar/Gait. Hemispheric lesions may produce a homonymous field defect and ipsilateral hemiparesis when the optic radiations and motor strip or descending motor fibers are disrupted. A proximal posterior cerebral artery occlusion causes a similar clinical picture by leading to infarction of the cerebral peduncle in the midbrain and of the occipital lobe. Signs of cerebellar dysfunction such as nystagmus, truncal or appendicular ataxia, dysmetria, intention tremor, dysdiadochokinesia, or scanning speech together with a congruous homonymous hemianopia suggest vertebrobasilar occlusion. Patients with multiple sclerosis presenting with optic neuritis may have cerebellar signs indicating previous white matter involvement. Any process affecting both the afferent visual pathways and corticospinal tracts can cause visual loss and hyperreflexia. For instance, large hemispheric lesions can be expected to result in contralateral hemianopia and hyperreflexia. Conditions affecting central myelin (e.g., multiple sclerosis or acute disseminated encephalomyelitis) can cause optic or chiasmal neuropathy as well as spasticity and hyperreflexia. In central and peripheral dysmyelinating syndromes, there may be visual loss and hyporeflexia.

Sensory. A homonymous field defect in combination with ipsilateral sensory loss, astereognosis, decreased two-point discrimination, or graphesthesia suggests a parietal lesion. A process within the nondominant (usually right) parietal lobe can also produce a contralateral neglect syndrome or hemianopia, accompanied by contralateral sensory inattention. Pain, hemianesthesia, or choreoathetoid movements and an ipsilateral homonymous field deficit imply co-involvement of the thalamus and optic radiations.

Autonomic Nervous System. Autonomic system dysfunction, primarily because of pupillary and lacrimal disturbances, may lead to visual complaints. For instance, patients with pathological mydriasis due to parasympathetic dysfunction can suffer from photophobia or refractive error. The latter results from exposing spherical aberrations in the lens and cornea. Tonic pupils (Adie's pupils, for instance) are associated with accommodative insufficiency, and patients may complain of difficulty reading. Lacrimation abnormalities cause dry corneas, resulting in hazy views with irritative symptoms that are responsive to topical lubrication. Horner's syndrome (oculosympathetic dysfunction), by itself, should not cause visual abnormalities.

Neurovascular. Amaurosis fugax due to carotid stenosis may be associated with a carotid bruit, although that finding is notoriously unreliable. Cranial or ocular bruits may indicate an intracranial arteriovenous malformation or a carotid-cavernous fistula. In some instances of visual loss due to anterior ischemic optic neuropathy, underlying giant cell arteritis is suggested by tender, cord-like temporal arteries.

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