Welcome to the clinical neurology podcast, where you will learn over 12 episodes how to localise a lesion in neurology based on history taking and physical examination. The podcast is meant for medical students and to make them enjoy learning neurology. Medicine, paediatrics, psychiatry, critical care, neurology residents, general practitioners and nurse practitioners will find it beneficial. Notes, images and other clinical resources for the podcast are available in the show description and on the neurology teaching club.com website. I am your host, Dr Krishnadas N C, and let’s get started.
In this episode, we will learn the functions of the various lobes of the brain. We will do that with the help of clinical cases. It won't be a comprehensive discussion on the lobe functions but an introduction to the fascinating world of cognitive neuroscience.
Let us start with a case. A 50-year-old banker was brought by his family to the neurology outpatient department with six months history of progressive cognitive decline. Premorbidly he was a hard-working polite family loving gentleman. The first symptom noticed was that he became rude and over-talkative to his colleagues. He commented about the dress of the female staff, which was not of his nature. One day he was found watching porn in his office. When enquired about it by seniors, he was very casual and didn't look embarrassed or apologetic. At home, he got angry with the kids quickly. When his wife fell ill, he didn't bother to take care of her or enquire about it. He needed to be coaxed to brush his teeth and bathe daily. He had a newfound liking for sweets and started to spend a lot of money on the online lottery. He started a car washing service near his home, far from the highway, which was shut down two months later. He almost met with an accident, as he was not looking to either side before crossing the road. With these symptoms, he was taken to a psychiatrist and referred to neurology.
This case illustrates most of the clinical features of frontal lobe dysfunction. There are three frontal circuits associated with cognition. These include
- Dorsolateral prefrontal
- Orbitofrontal
- Anterior Cingulate
The dorsolateral prefrontal circuit is responsible for attention, working memory and executive function. Dysfunction in this circuit is linked to environmental dependency syndromes like utilization and imitation behaviour, poor planning, mental inflexibility, and deficits in working memory. The lack of planning in starting a business where the patient has no experience in a remote area is a classic example of executive dysfunction. The orbitofrontal circuit is responsible for our personality, behaviour and emotional states. Lesions are associated with impulsivity, disinhibition, aggression, socially inappropriate behaviour, and mental inflexibility. His change in behaviour at home and office and lack of empathy when his wife was sick suggest orbitofrontal involvement. The anterior cingulate or mesial frontal circuit is essential in pursuing and regulating goal-oriented behaviour. Lesions of the anterior cingulate circuit cause the spectrum of amotivational syndromes, namely apathy, abulia, and akinetic mutism. It also causes cognitive impairment, including poor response inhibition, error detection, and goal-directed behaviour. The patient needed to be coaxed to brush his teeth and bathe are examples of anterior cingulate involvement.
The detailed lobe function examination showed involvement of the frontal more than the temporal lobe, and the MRI brain showed atrophy of the frontal and temporal lobe consistent with the clinical diagnosis of frontotemporal dementia.
A 75-year-old retired school teacher presented with forgetfulness of 6 months duration. He will forget where he kept his purse, look for it, and blame his wife for misplacing it. He will fail to pass messages told by his children over the telephone to his wife. While making tea, he will not put sugar or, at other times, add it twice. He could not tell the names of his grandchildren and distant relatives. While speaking, he often loses the flow and asks what was he talking about.
The patient has episodic memory impairment, which is responsible for his misplacing object, errors in cooking and failure to pass on messages. The episodic memory impairment is localized to the mesial temporal lobe, especially the hippocampus.
The detailed lobe function examination showed temporal more than parietal more than frontal lobe involvement. MRI showed severe atrophy of the temporal lobe consistent with the clinical diagnosis of Alzheimer's disease. Alzheimer's disease is a neurodegenerative disease which affects the medial temporal lobe early. So memory, mainly episodic memory, is impaired early. As the disease evolves, other lobes like the parietal and frontal also get involved.
A 60-year-old engineer presented with a history of difficulty recognizing his friends and relatives for six months. He came for consultation as he could not recognize his niece when she visited him. He talked to her for around 30 minutes and, after she left, asked his wife who she was. The rest of the history was normal except for an occasional word-finding difficulty. On examination, it was found that he had significant prosopagnosia or problem-identifying faces. He could not recognize famous movie actors and political leaders but could identify them by hearing their voices. Semantic word knowledge was grossly impaired during the neurocognitive testing, to the surprise of himself and his family members. Semantics refers to the meaning of words. He could not understand what a wash basin was or describe it. He struggled with category fluency, like naming seven animals but did well in verbal fluency, like words starting with p, again suggesting loss of semantics. The prosopagnosia is localized to the fusiform gyrus and semantics to the anterior and lateral temporal lobes. The possibility of semantic dementia, a variant of frontotemporal dementia, was considered, and the differential kept in mind was the posterior cortical atrophy variant of Alzheimer's disease. Both of these can present with prosopagnosia. The MRI brain showed significant atrophy of the bilateral temporal lobe left more than right, consistent with the clinical diagnosis of semantic dementia. The above two cases summarise the main functions of the temporal lobe, namely episodic memory in the hippocampus, face recognition in the fusiform gyrus and semantic memory in the anterior and lateral temporal lobe.
A 63-year-old farmer presented with slowness of activities and abnormal posturing of the right upper limb. He had significant difficulty doing day-to-day activities like brushing his teeth, unlocking a door or switching on a fan. On examination, he could not pantomime like waving bye-bye with his right upper limb, and he struggled to open a lock with a key. He was holding the key abnormally and could not even insert the key into the hole in the lock, suggesting apraxia. Apraxia is the inability to do a learned motor activity in the absence of weakness, ataxia, sensory impairment, abnormal tone or involuntary movements. Apraxia can be caused by lesions involving the dominant inferior parietal lobule or left supplementary motor cortex, corpus callosum or right supplementary motor cortex. The lesions at these various sites produce various types of apraxia. The patient had stimulus-sensitive myoclonus. He had cogwheel rigidity, dystonia and cortical sensory loss on the right side. A provisional diagnosis of parkinsonian plus syndrome coritico-basal syndrome was considered, and the MRI brain showed asymmetrical atrophy of the left parietal lobe consistent with the clinical diagnosis. The major function of the left parietal lobe functions is praxis, and the lesion causes apraxia. The angular gyrus forms the posterior part of the inferior parietal lobe. Damage to the left angular gyrus by stroke or tumour causes the classic Gerstmann syndrome. It includes acalculia or difficulty in calculation, agraphia or difficulty writing, finger anomia, and right-left disorientation. A right parietal lesion will produce hemineglect of the left side, constructional and dressing apraxia and topographical disorientation.
A 55-year-old housewife, known diabetic and hypertensive, presented with new onset visual symptoms in the morning. She said she could not see things correctly. On examination, the fundus was normal, and pupils were equal and reacting to light. While testing vision, she could not identify a pen while seeing it. She could see it but could not recognize it. She could match it with a picture of a pen but still could not identify it or tell its use. On holding the pen in her hand, she could immediately recognize it as a pen and describe its use. She was diagnosed with associative visual agnosia, and an MRI brain showed an acute infarct involving the left occipital cortex and corpus callosum. In visual agnosia, the patient fails to recognize objects by sight, with preserved ability to recognize them through touch or hearing. The vision should be normal, and the patient should not have other cognitive problems. There are various types, like apperceptive and associative depending on the severity of visual agnosia. It is caused when the information from the visual cortex fails to reach the semantic conceptual field, so the meaning of the visual image cannot be understood. Bilateral occipital infarct can cause cortical blindness, and unilateral occipital infarct can cause homonymous hemianopia on the opposite side.
These cases discussed some of the major clinical features of lesions involving the various lobes of the brain. A detailed history will often reveal these clinical findings, and a thorough neurocognitive assessment will confirm them. In advanced dementia, the neurocognitive assessment will show involvement in all the lobes. Only from history will we be able to tell which lobe was first involved, which is very important to making the diagnosis. For example, in Alzheimer's disease, the temporal is involved early, followed by parietal, frontal and occipital. In frontotemporal dementia, the frontal lobe is first affected, followed by the temporal, parietal and occipital lobes. Ultimately, the diagnosis boils down to how good your history is.
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