Chapter 2 - Presenting signs and symptoms in brain tumors
Introduction
The era of sophisticated and ubiquitous neuroimaging has made many of the clinical distinctions regarding differential diagnosis and localization by semiology rather moot. A detailed investigation regarding the specific etiology of intracranial mass lesions is not well informed by mode of clinical presentation, but much more on epidemiologic and imaging features rather than clinical symptomatology.
A mixture of mechanisms causes the symptoms and signs and their combination produces the clinical syndromes observed in patients (DeAngelis et al., 2002). Jaeckle (1998) reported in the last update to this volume that much of the localizing symptomatology of brain tumors is not specifically tied to specific tumor types, but rather by location within the nervous system. Tumor can damage neural tissue or displace it by compression, leading to focal symptoms. Direct invasion of the tumor typically occurs in infiltrating gliomas or lymphomas, whereas meningiomas and metastases displace brain tissue. The disruption of the blood–brain barrier by the tumor leads to vasogenic edema that is probably one of the main causes of clinical impairment. Edema favors an increased mass effect and thus further compression of the surrounding brain. Furthermore, presenting symptomatology can be often attributed to more generalized symptoms and signs, including headache, altered mental status, seizure and symptoms of increased intracranial pressure, including papilledema, nausea, and vomiting.
As detailed elsewhere, there are also detailed descriptions of the evolution of symptoms associated with various herniation syndromes, but again, these are not specific to tumor, but can be seen with any intracranial mass lesion. As a result, these are not necessarily helpful for diagnosis, whereas neuroimaging can quickly distinguish most responsible lesions.
Mechanisms of presenting symptomatology can be divided into tumor and peritumoral factors. Tumor factors include histology, for example, in that seizures are common in patients with certain low-grade gliomas. Rapidly growing high-grade tumors may cause more widespread tissue destruction, whereas more indolent tumors may cause partial deafferentation of cortical neurons, with resulting denervation hypersensitivity and hence a more epileptogenic microenvironment.
Tumor location is obviously critical regarding symptomatology, but certain locations are closely related to certain histologies and can suggest the relative likelihood of certain tumors. Glioneuronal tumors and astrocytomas appear to favor the temporal lobes and oligodendrogliomas may more likely be located in frontal lobes. It is not clear whether these location correlations have any neurodevelopmental or mechanistic basis.
Peritumoral factors, including regional hypoxia blood–brain barrier breakdown, may predispose to seizure and localized neuronal dysfunction. Ionic changes in the peritumoral zone may influence neuronal activity and extracellular glutamate may be associated with neuronal hyperexcitability.
Section snippets
Headache
Prospective studies and retrospective case series have attempted to assess the risk of intracranial mass or neoplasm in patients presenting with headache. Interestingly, it is important to note that the prevalence of brain imaging abnormalities on magnetic resonance imaging is low in patients without headache. A meta-analysis of 16 studies (n = 19 559) showed a prevalence of asymptomatic brain neoplasm of 0.7% (95% confidence interval, 0.47–0.98%) (Morris et al., 2009). The American Academy of
CSF obstruction
The classic presentation of cerebrospinal fluid (CSF) obstruction was described by Dandy in 1922 in a case of third ventricular colloid cyst with intermittent obstruction and positional recumbent headache. Nevertheless, it should be noted that a prospective study of 105 colloid cysts of the third ventricle found only 2 patients with positional headache (Desai et al., 2002). Generalized intermittent headache was present in 92.3% of patients, with associated ataxia (25.7%), blurred vision (20%),
Localizing symptoms and signs of intracranial neoplasms
Localizing symptoms and signs of intracranial neoplasms can differ based on the relative preponderance of lesions responsible, but these are typically only relatively specific. Patterns of growth, either bulk growth or infiltrative growth, may also impact the evolution of clinical symptoms and signs (Biller et al., 2011).
Stroke-like presentation may be due to intratumoral hemorrhage, but rapid symptom onset and evolution may also be seen in evolving mass effect even without sudden intratumor
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2018, Handbook of Clinical NeurologyCitation Excerpt :Seizures can generally be grouped into partial and generalized types. Focal seizures will cause a variety of symptoms based on their location, histology, and other peritumoral factors (Alentorn et al., 2016). Although the pathophysiology is not well understood, patients with brain metastases tend to present with more focal motor seizures (Newton, 1999).
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