Frontal Lobe Syndrome

Frontal lobe syndrome (FLS) is widely onomastion used to describe damage of advanced functional brain processes such as social behavior, planning, motivation, and language/speech production. It usually refers to a clinical syndrome caused by impaired prefrontal lobe function. The related prefrontal lobe regions may include the anterior cingulate, lateral prefrontal cortex, orbitofrontal cortex, and frontal lobe pole.

Histopathology

FLS induced by neurodegenerative disorders are usually caused by two major histopathological factors: α-synuclein and tau protein. Tauopathies with frontal lobe damage include frontotemporal dementia, chronic traumatic encephalopathy, supranuclear palsy, corticobasal degeneration (CBD), and advanced AD. If tau protein is over phosphorylated, the protein will be separated from microtubules to produce insoluble aggregates. The Braak stages classify the extent of neurofibrillary tangles. Contrary, α-synuclein is associated with multiple system atrophy, Parkinson's disease, and diffuse Lewy body dementia.

Fig.1 Prefrontal cortex. (Pirau, 2020)

Pathogenesis of FLS

The pathogenesis of frontal lobe disorders entails various pathologies, some are as follows:

• Frontal abulic syndrome

Emotional apathy and flatness. Loss of initiative, creativity, and curiosity. Akinetic mutism.

• Frontal disinhibition syndrome

It is caused by injury to the frontal lobe, usually by tumors. Social disinhibition, judgment, insight, and foresight can be severely impaired. Frontal disinhibition syndrome is typically characterized by antisocial behavior.

• Foster-Kennedy syndrome

It is caused by frontal lobe tumors, causing ipsilateral optic atrophy and contralateral optic papilledema.

Evaluation of FLS

Before a diagnosis of FLS, it is important to rule out other possible causes of cognitive damage, for example, B12, thyroid function, and syphilis serology if applicable. In terms of imaging, MRI can be used to assess atrophy, hematomas, vascular and microvascular pathology. CT, while not specific or sensitive, can rule out acute hemorrhage or hydrocephalus. If frontotemporal dementia (FTD) is clinically suspected, neurologists may consider performing a deoxyglucose PET scan that shows reduced frontal lobe activity and retention of the temporoparietal region.

Fig.2 CT axial image showing subcortical calcifications having a characteristic “tram-track”-like appearance in the left frontal, parietal, and occipital lobes with atrophy of cerebral cortex involving the left frontal lobe to a greater extent. (Ragupathi, 2014)

The Use of Biomarkers in Differentiating Between FLS Causes

After taking a detailed history and a physical exam, more discriminating instruments might be needed to differentiate between FLS causes. Measuring cerebrospinal fluid (CSF) levels of amyloid-beta, total tau, and phosphorylated tau (p-tau) is mainly helpful to distinguish FTD from AD, but no specific pattern is found in other causes of FLS.

In psychiatric disorders like depression and schizophrenia, CSF biomarker results have been found to vary between normal to slightly elevated total-tau and p-tau levels compared to healthy controls but significantly lower than seen in AD.

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References

1. Pirau, L.; Lui, F. Frontal Lobe Syndrome. StatPearls Publishing, Treasure Island (FL). 2020. PMID: 30422576.
2. Ragupathi, S.; et al. Sturge-Weber syndrome: CT and MRI illustrations. BMJ Case Rep. 2014.