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Neurology > Cerebrum & Dementia > Flashcards

Cerebrum & Dementia Flashcards

1
Q

What are the two broad parts of the cerebrum?

A
  • the cerebrum/forebrain/prosencephalon develops into two sub groups: the telencephalon (hemispheres, basal ganglia, lateral ventricles, etc.) and the diencephalon (epithalamus, thalamus, hypothalamus, and ventral thalamus, and 3rd ventricle)
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2
Q

What separates the two cerebral hemispheres? What connects them?

A
  • they are separated by the great longitudinal fissure

- they are connected by the corpus callosum (commissural fibers)

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3
Q

What separates the frontal lobe from the parietal lobe? What separates the frontal and parietal lobes from the temporal lobe?

A
  • central sulcus separates frontal from parietal

- lateral fissure separates frontal and parietal from temporal

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4
Q

What is the gyrus just anterior to the central sulcus called? What about that just posterior to the central sulcus?

A
  • anterior: precentral gryus - contains the primary motor cortex
  • posterior: postcentral gyrus - contains the primary somatosensory cortex
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5
Q

Where is the primary auditory cortex located?

A
  • in the superior temporal gyrus of the temporal lobe
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6
Q

What are the three types of signs/symptoms that focal cerebral lesions can cause?

A
  • focal epileptic seizures (due to repetitive discharging of the affected neurons)
  • sensory/motor deficits (due to involvement of respective cortices)
  • psychological deficits (due to loss of brain matter dealing with language, memory, perception, etc.)
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7
Q

What does a unilateral cerebral hemisphere lesion result in? What can rapidly cause such a lesion?

A
  • mental impairment, contralateral spastic hemiparesis + hyperreflexia + Babinski positive (extensor plantar response), contralateral hemisensory loss
  • a stroke can cause a rapid unilateral cerebral hemisphere lesion
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8
Q

How many layers does the cerebral cortex have? In which layer do afferents from the thalamic nuclei project to? From which layer do projection fibers/tracts (to subcortical structures) originate?

A
  • cortex has 6 layers (I to VI, running superficial to deep)
  • thalamic nuclei project to layer IV
  • projection fibers originate in layer V
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9
Q

What are association centers/cortices?

A
  • these are areas between adjacent gyri/lobes that permit multimodal identification of objects, sensations, etc.
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10
Q

What do the medial portions of the cerebrum deal with?

A
  • this is the limbic system (made up of the hippocampus, cingulate gyrus, and parahippocampal gyrus); it enables storage and retrieval of information
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11
Q

Which hemisphere is usually responsible for language?

A
  • most individuals are left hemisphere dominant, meaning language is generated in the left hemisphere’s association cortices
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12
Q

Describe the layout of the primary motor homunculus in the primary motor cortex.

A
  • moving superiorly/medially: larynx, pharynx, tongue, nose, eyes, neck, fingers, hands, shoulders, trunk, hips, knees, legs, foot, genitals
  • the larynx, tongue, face, and fingers have the largest regions
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13
Q

The primary motor cortex receives afferents from mainly which thalamic nuclei? What about the premotor cortex?

A
  • primary motor cortex: ventral lateral (VL) nucleus of thalamus
  • premotor cortex: ventral anterior (VA) nucleus of thalamus
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14
Q

Where is the premotor cortex? Which cortex is contained within it?

A
  • premotor cortex is immediately anterior to the primary motor cortex
  • within the premotor cortex lies the supplementary motor cortex
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15
Q

What lies anterior to the premotor cortex?

A
  • in both hemispheres, the frontal eye field gyrus is found anterior to the premotor cortex
  • in the dominant hemisphere, Broca’s area is also found here (this is the motor speech gyrus, deals with word formation)
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16
Q

What will result from a left frontal lobe lesion?

A
  • right-sided focal seizures, right-sided UMN lesions, speech deficit (expressive/Broca’s aphasia: patient understands language, knows what he wants to say, but is unable to do so; extremely poor articulation and loss of fluency; they are aware of their disability), dementia
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17
Q

What lies anterior to the all the motor cortices?

A
  • the prefrontal cortex: controls intellectual, judgmental, and predictive faculties and behavior (executive function)
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18
Q

The primary somatosensory cortex receives afferents from mainly which thalamic nuclei?

A
  • the ventral posterolateral (VPL) nucleus of the thalamus
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19
Q

What will result from a left parietal lobe lesion? A right parietal lobe lesion?

A
  • left: right-sided focal seizures, right-sided hemisensory loss, right-sided inferior visual field loss, inability to name objects, loss of literacy (reading and writing) and calculation
  • right: left-sided focal seizures, left-sided hemisensory loss, left-sided inferior visual field loss, spatial disorientation
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20
Q

The primary auditory cortex (in the temporal lobe) receives afferents from mainly which thalamic nuclei? What is unique about these afferent fibers?

A
  • the medial geniculate nucleus (MGN) of the thalamus
  • these fibers partially decussate as they ascend to the cortex, meaning that they have bilateral representation; a lesion in one temporal lobe will, therefore, result in partial deafness in both ears
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21
Q

What is located posteriorly to and surrounding the primary auditory cortex in the temporal lobe?

A
  • the auditory association cortex; in the dominant hemisphere (usually left) this is called Wernicke’s area (deals with language comprehension and word choice)
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22
Q

What will result from a left temporal lobe lesion?

A
  • right-sided focal seizures, right-sided superior visual field loss, bilateral partial deafness, speech deficit (receptive/Wernicke’s aphasia: patient can’t understand written or spoken language; speech is fluent but non-sensical; often they are unaware of their difficulty speaking)
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23
Q

What is found in the calcarine sulcus in the occipital lobe? What’s found in the rest of the lobe?

A
  • the primary visual cortex

- the rest of the occipital lobe contains the visual association cortex

24
Q

The primary visual cortex receives afferents from mainly which thalamic nuclei?

A
  • the lateral geniculate nucleus (LGN) of the thalamus
25
Q

What is represented in each primary visual cortex?

A
  • each primary visual cortex deals with the lateral half of the visual field of the contralateral eye
26
Q

What will result from a left-sided occipital lobe lesion? A bilateral lesion?

A
  • focal seizures and right-sided lateral visual field loss
  • if bilateral: cortical blindness (partial or total bilateral vision loss; often the patient will deny the vision loss!)
27
Q

The left hemisphere is usually dominant for what processes? What about the right hemisphere?

A
  • left: language and mathematics (logical), recognition of local features
  • right: spatial perception, emotion, and musical proficiency (creative), recognition of global features
28
Q

What are the three types of fibers found in the white matter of the cerebral hemispheres?

A
  • association fibers: connecting cortical sites within one hemisphere (back and forth)
  • commissural fibers: connecting related sites of one hemisphere to the other (left and right)
  • projection fibers: connecting subcortical structures with the cortex (up and down)
29
Q

What are the major association fibers of the cortex?

A
  • superior longitudinal fasciculus: connects frontal, temporal, and occipital
  • arcuate fasciculus: connects frontal and temporal (connects Broca’s and Wernicke’s areas; important for language)
  • inferior longitudinal fasciculus: connects occipital and temporal (important for visual recognition)
  • uncinate fasciculus: connects frontal and temporal (important for behavior)
  • cingulum: connects lobes with limbic system
30
Q

What is the anterior commissure?

A
  • essentially a smaller version of the corpus callosum
  • this is made up of commissural fibers that link the two temporal lobes
  • the temporal lobes are not connected via the corpus callosum!
31
Q

What does damage to the corpus callosum result in?

A
  • results in relatively normal function, but in a disconnected fashion
  • (ex: patient can write normally, but can’t read)
  • (ex: visual info to the non-dominant side will not evoke a verbal response)
32
Q

What is prosody?

A
  • prosody is the concept of language conveying emotion
  • this means that lesions of the right hemisphere WILL impact the patient’s language (flattened intonation and difficulty in judging other’s emotional tone, sarcasm, etc.)
33
Q

How long is short-term memory? What about long-term? Which lobes are involved in each?

A
  • short-term: seconds to minutes; frontal lobe (the prefrontal cortex)
  • long-term: hours to years; temporal lobes (with the hippocampus)
34
Q

What are the two types of long-term memory?

A
  • explicit (AKA declarative) memory: facts, events, autobiographical memory; knowledge, reflective tasks, conscious recall
  • implicit (AKA non-declarative) memory: habits, skills, priming and conditioning; motor skills, reflexive tasks, unconscious recall
35
Q

Which structure plays a vital role in developing learned emotional responses (such as fear)?

A
  • the amygdala (plays a role in recognizing our own and others’ emotional responses)
36
Q

Alzheimer’s Disease

A
  • the most common cause of dementia (60%) in the elderly population
  • this is diffuse degeneration of the brain parenchyma resulting in an insidious onset of impaired higher intellectual function and altered mood/behavior that progresses to disorientation, memory loss, and profound disability + muteness
  • most common deficits: short-term memory loss with variable dysfunction of executive function, visuospatial function, and language
37
Q

What gross morphology do we see in Alzheimer’s Disease? What microscopic characteristics?

A
  • gross: widening of the sulci and gyral atrophy due to loss of brain parenchyma, with resulting dilated ventricles (hyrdocephalus ex vacuo)
  • microscopic: beta amyloid plaques (extracellular) and tangles of Tau (intracellular)
  • (Tau is a neuronal microtubule binding protein; when it is phosphorylated it relocates from the axons to the cell bodies, where it aggregates into tangles)
38
Q

What is dementia? In contrast, what is delirium?

A
  • dementia: a progressive degradation in intellectual function that impairs social/occupational functioning
  • delirium (AKA acute confusional state or acute brain syndrome): a transient state of confusion due to some underlying cause (infection, drugs, intoxication, etc.)
  • (EEG for delirium: classic wide-spread slow-wave activity)
  • patients with dementia have an increased susceptibility to developing delirium
39
Q

When does Alzheimer’s classically begin? How common is it? What are the main risk factors? Is anything thought to be protective?

A
  • Alzheimer’s usually begins after 60
  • it initially has a 1% prevalence, but this doubles every 5 years (so by 85 it’s between 30 and 50%)
  • risk factors: age, family history, diabetes (and other vascular disorders), history of significant/repeated head trauma, ApoE epsilon 4 isotope, Down syndrome, poor education, depression
  • protective: ApoE epsilon 2 isotope, good education, social interaction, NSAIDs, statins, light alcohol consumption
40
Q

Degeneration of the hippocampus will result in what? What about the left tempoparietal junction? The right parietal lobe? The left parietal lobe? The frontal lobe?

A
  • hippocampus: short-term memory loss
  • left tempoparietal junction (Wernicke’s area): word-finding difficulty, receptive dysarthria)
  • right parietal lobe: visuospatial dysfunction (getting lost, not recognizing faces, etc.)
  • left parietal lobe: apraxia
  • frontal lobe: executive dysfunction (easily distracted, mentally inflexible, etc)
41
Q

What investigations should be done in a patient presenting with a new cognitive complaint?

A
  • brain imaging is indicated in all cases; the goal here is to rule out cerebrovascular disease, tumor, or other structural abnormality (rather than to confirm Alzheimer’s)
  • MRI is the best, but CT is OK as well; can do a PET scan as well to show hypometabolic areas of Alzheimer’s)
42
Q

How do we treat Alzheimer’s Disease?

A
  • encourage aerobic exercise, social/community involvement, and frequent mental stimulation
  • 1st line drug therapy: cholinesterase inhibitors (donepezil, rivastigamine, galantamine): mildly treat the cognitive impairment (these will NOT prevent disease progression); side effects: nausea and diarrhea are common, syncope and arrhythmia are uncommon
  • NMDA-receptor antagonists (memantine) work similarly
  • can give selective serotonin reuptake inhibitors (SSRIs) to treat depression, anxiety, and agitation; also give anticonvulsants (carbamazepine) and antipsychotics
43
Q

What can cause an immensely rapidly progressive dementia (weeks to months)?

A
  • Creutzfeldt-Jakob disease (CJD) via an “infection” with a prion (can also arise sporadically)
  • the normal degradable protein is PrPc; prion form is PrPsc (forms beta-pleated sheets; which are resistant to proteases)
  • (CJD is the most common form of spongiform encephalopathy, which is degeneration due to prion protein accumulation)
  • (vCJD is variant CJD, due to consumption of contaminated meat; “mad cow disease”)
44
Q

What are the two major causes of dementia? What are some others? What percent of cases are reversible?

A
  • degenerative disorders (AD alone makes up 50-60% of all cases) and vascular disruptions (11% of all cases); 21% are mixed Alzheimer’s + vascular
  • others: infection (CJD), systemic inflammatory disease, neoplasm, trauma, iatrogenic (anticholinergics and antihistamines), normal pressure hydrocephalus, etc.
  • 10-20% of cases are due to reversible causes
45
Q

What are the major degenerative disorders leading to dementia?

A
  • Alzheimer’s disease (AD) is the major one
  • dementia with Lewy bodies (DLB), frontotemporal dementia (FTD), end-stage Parkinson’s disease, end-stage Huntington’s disease
  • (DLB is essentially dementia and Parkinsonism developing at the same time)
46
Q

What type of heterogeneity is involved in Alzheimer’s Disease?

A
  • locus heterogeneity (where several genes can cause the disease)
  • as opposed to allelic heterogeneity (where only a single gene causes the disease) as seen in Huntington’s
47
Q

What is the proposed pathogenesis of Alzheimer’s disease?

A
  • accumulation of beta amyloid proteins
  • these result from alternative cleavage of the APPs (amyloid precursor proteins); normally, APP is cleaved by alpha-secretase into a degradable byproduct, but occasionally, they get cleaved by beta-secretase, generating Abeta40/42 fragments (these are unable to be cleared, and accumulate into plaques)
  • the Abeta40 fragment tends to be more benign, while the Abeta42 fragment is associated with a more rapid onset and progression of the disease
48
Q

What percentage of Alzheimer’s cases are clearly familial? Which genes are mainly involved?

A
  • less than 2-5% of cases of AD are clearly familial; all cases so far are A.D. and involve chromosome 1, 19, or 21
  • chromosome 14’s PSEN1 gene is most commonly mutated
  • chromosome 1’s PSEN2 gene is more rare
  • chromosome 21 contains the APP gene (thus patients with Down syndrome - trisomy 21 - nearly always develop Alzheimer’s)
  • (mutated PSENs or APP genes result in altered processing of the APP protein)
49
Q

Explain the role of ApoE in Alzheimer’s disease.

A
  • (apolipoprotein E)
  • three variants: epsilon2, epsilon3, and epsilon4
  • epsilon3 is the wild type, with 1 cysteine and 1 arginine
  • epsilon2 protects against AD, with 2 cysteines
  • epsilon4 predisposes to AD, with 2 arginines (increases the conversion of APP to the non-degradable form)
50
Q

DDx of Dementia

A
  • delirium, aphasic stroke, severe depression with pseudodementia, amnestic disorder (such as Wernicke-Korsakoff), intellectual impairment
51
Q

How do we diagnose Alzheimer’s Disease? How about vascular dementia?

A

1) patient has memory impairment and at least one of the following: aphasia, apraxia, agnosia (difficulty recognizing objects/faces), executive dysfunction
2) dysfunction must impair social/occupational setting
3) must not be due to delirium or another disease
- vascular: above 2 points + focal neurological signs or lab evidence of cerebrovascular disease

52
Q

Vaccine for Dementia

A
  • (not yet approved)
  • vaccine against the Abeta42 protein results in clearing of the neuritic plaques!
  • this works in mice
  • works in humans, BUT 6% developed meningoencephalitis with an auto-antibody reaction to brain tissue
53
Q

What do most patients with Alzheimer’s Disease die from?

A
  • 57% die from pneumonia
  • 16% from cardiovascular disease
  • 14% from PE
54
Q

What characterizes an amnestic disorder? What are common causes?

A
  • severe impairment of new learning ability and an inability to recall previous memories WITHOUT a general loss of intellectual ability (vs. dementia) and WITHOUT clouding of consciousness (vs. delirium)
  • common causes: Wernicke-Korsakoff syndrome, head trauma, brain tumor, subarachnoid hemorrhage, CO poisoning, encephalitis
55
Q

What is Pick disease?

A
  • a type of frontotemporal dementia characterized by Pick bodies (round aggregates - NOT tangles - of Tau)
56
Q

What is the Charcot classic triad of presentation of multiple sclerosis?

A
  • “S.I.N.”
  • Scanning speech
  • Intention tremor (or Incontinence, or Internuclear ophthalmoplegia)
  • Nystagmus

Neurology (18 decks)

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