The Neuropsychology of Cancer and Oncology by Chad A. Noggle PhD ABN & Raymond S. Dean PhD ABPP ABN

The Neuropsychology of Cancer and Oncology by Chad A. Noggle PhD ABN & Raymond S. Dean PhD ABPP ABN

Author:Chad A. Noggle, PhD, ABN, & Raymond S. Dean, PhD, ABPP, ABN
Language: eng
Format: epub
Publisher: Demosmed Pub
Published: 2013-03-17T16:00:00+00:00


FIGURE 11.2 Syndromes related to neoplastic involvement of brain structures or neurologic complications of cancer therapy. (A). Patient with Anton syndrome evolving in a patient with radiation necrosis after radiosurgery for a progressive bi-occipital meningioma. (B). Complex diencephalic syndrome characterized by diabetes insipidus and morbid obesity in a patient with hypothalamic Non-Hodgkin lymphoma. (C). This patient with left a prefrontal astrocytoma developed a transient left supplemental motor area syndrome after subtotal resection. (D). Severe cerebellar syndrome resembling cerebellar mutism in an adult patient after resection of medulloblastoma followed by craniospinal irradiation.

Brainstem tumors, especially when infiltrative and malignant, cause rapidly progressive syndromes comprised of nuclear or fascicular cranial neuropathies and crossed long tract signs. Parenchymal invasion of the mesencephalon is the basis for nuclear third nerve palsies. Infiltration of the corticospinal tract, spinothalamic tract, and fasciculus longitudinalis medialis give rise to contralateral hemiparesis, sensory loss with allodynia and internuclear ophthalmoplegia, respectively. Invasion of the area postrema is the basis for intractable nausea. A peculiar syndrome arises from tumors growing along the craniocaudal axis of the brainstem while respecting the midline of the brainstem. This growth pattern gives rise to cranial nerve dysfunction restricted to one side (Garcin syndrome). The small size of the infratentorial compartment results in early signs of spinal fluid obstruction or upward or downward herniation. Appendicular ataxia characterizes cerebellar hemispheric lesions while midline tumors predominantly affect stance and gait.

A peculiar syndrome comprised of seizures, hemiparesis, or aphasia is frequently observed after operations within the supplementary motor area (SMA; Figure 11.2C). The severity of the SMA syndrome is dependent upon extent of resection. While frequently dramatic upon awakening from anesthesia, it is fully reversible within days to weeks (Zentner, et al., 1996). Transient mutism is a complication of cerebellar tumor resection in children (Figure 11.2D; Rekate et al., 1985).

Constitutional complaints such as fatigue, psychomotor slowing, altered appetite, and anosmia characterize early effects of radiation therapy. The somnolence syndrome is characterized by excessive drowsiness, an inability to concentrate, lethargy, mental slowness, and fatigue (Faithfull & Brada, 1998). Vasogenic cerebral edema and radiation necrosis lead to signs and symptoms of increased intracranial pressure and worsening of focal neurological deficits. A neurodegenerative disorder resembling Binswanger’s disease or the classical triad of subcortical dementia, gait apraxia, and cortical bladder dysfunction seen in normal pressure hydrocephalus is encountered in long-term survivors of WBRT (Lai et al., 2004). Endocrinopathies arise from irradiation of the hypothalamus and pituitary region. Secondary tumors within the radiation field (meningioma, malignant glioma, primitive neuroektodermal tumor) may give rise to similar syndromes experienced at the time of original tumor diagnosis for which ionizing radiation was administered.

Various neuropsychiatric syndromes have been described after specific chemotherapies or polychemotherapy regimens. DLEPS presents as a stroke-like syndrome or as global encephalopathy. Patients develop seizures, severe headache, or transient focal neurological symptoms (sensory disturbance, aphasia, weakness). Symptoms in DLEPS may fluctuate over a few days and spread to involve both hemispheres but then generally resolve without clinical residual (Baehring & Fulbright, 2008). Posterior reversible encephalopathy syndrome presents with headache, cortical blindness, altered mental status, and seizures.



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