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MHD- Neuro > Random Associations from all of the Lectures > Flashcards

Random Associations from all of the Lectures Flashcards

1
Q

If someone has a few episodes of “dark shade lowering in one eye”, what is this a warning sign for? What is the “dark shade” called?

A

Amaurosis Fugax

This is a symptoms of a TIA in the internal carotid territory. Warning signs that the ipsilateral internal carotid artery is at risk for a full on stroke.

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2
Q

What symptoms of a TIA indicate the vertebrobasilar artery is at risk of a stroke?

A

Brainstem or cerebellar syndromes (ataxia, diplopia), visual cortex involvement such as homonymous hemianopsia

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3
Q

Dominant (left) sided infarcts leads to which hemispheric disorder?

A

Aphasia- inability to communicate

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4
Q

Non-dominant (right) sided infarcts leads to which hemispheric disorders?

A

hemineglect and anosognosia

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5
Q

Differentiate causes of large vessel vs small vessel infarctions

A

Large vessel: either thrombotic or embolic–> hemispheric syndromes

Small vessel: only thrombotic (HTN) –> lacunar syndrome

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6
Q

When would you perform a carotid endarterectomy?

A

for SYMPTOMATIC flow-limiting cervical internal carotid artery (ICA) stenosis of 70% to 99%

No symptoms, no surgery necessary

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7
Q

What is the most common cause of cerebral hemorrhage?

A

Hypertension

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8
Q

What are typical bleeding sites of cerebral hemorrhage?

A

Thalamus, basal ganglia

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9
Q

`Cause of epidural bleeds?

A

Trauma to middle meningeal artery

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10
Q

Cause of subdural bleeds?

A

Trauma –> tearing of bridging veins

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11
Q

Cause of SAH?

A

Non-traumatic: berry aneurysm rupture

Traumatic is the most common cause overall–>

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12
Q

Cause of intraparenchymal bleeds?

A

HTN, AVM

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13
Q

Consequences of subfalcine herniation?

A

Rupture of ACA

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14
Q

Consequence of uncal herniation?

A

Duret hemorrhage (due to rupture of paramedian artery), compression of CN III, compression of PCA

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15
Q

Consequence of tonsillar herniation?

A

compression of brainstem –> cardiopulmonary arrest

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16
Q

What parts of the brain are involved in a coma?

A

Cerebral cortex is not functioning
Reflexes from the brainstem will be intact

If reflexes are gone, you’re braindead.

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17
Q

Withdrawl to painful stimuli on exam requires some function of what part of the brain?

A

The cortex

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18
Q

Differentiate the location of lesions leading to decorticate and decerebrate posturing

A

Decorticate: cerebral lesion

Decerebrate: lesion at midbrain (red nucleus)

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19
Q

How do breathing patterns localize to CNS lesions?

A

They don’t- they can’t precisely predict brain/brain stem infarctions

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20
Q

Which reflex is preserved in a metabolic coma even when the other reflexes are lost?

A

The pupillary light reflex

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21
Q

What is indicated by a large, fixed, “blown” pupil?

A

Uncal herniation and CN III compression. This is a neurologic emergency

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22
Q

What is the oculocephalic reflex?

A

“doll’s eyes” reflex: normally the eyes will passively move opposite to the direction of the head
Checks to make sure the brainstem is intact

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23
Q

What is required as a confirmatory test for brain death?

A

1) no brainstem reflexes can be present

2) absent cerebral blood flow over a 10 minute period of time on radioisotope brain scan

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24
Q

What is the general relationship between the basal ganglia, thalamus, and motor cortex?

A

Basal ganglia inhibits the thalamus
Thalamus stimulates the cortex
Cortex stimulates the basal ganglia

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25
How does Parkinson's disease lead to a hypokinesia?
Loss of dopamine leads to a net decrease in stimulation of the GPm. Net stimulation of GPm leads to increased inhibition of the thalamus, and less stimulation of the cortex
26
What causes hyperkinesia with hemiballismus?
Lesions of the SUBTHALAMIC NUCLEI lessons stimulation of the GPm. Less stimulation of GPm leads to less inhibition of the VL of the thalamus and over stimulation of the cortex
27
How does Huntington's disease lead to hyperkinesia?
Destruction of the caudate --> loss of the indirect pathway and less stimulation of GPm. Less stimulation of GPm leads to less inhibition of the VL of the thalamus and over stimulation of the cortex
28
Infarcts, hemorrhages, or tumors of the striatum or STN leads to what movement disorders?
Contralateral choreoathetosis or hemiballismus
29
Dopamine agonists lead to what types of movement disorders?
Hyperkinesia: chorea or dystonia
30
What generally causes asterixis?
Metabolic disorders
31
What are the 4 motor disturbances in parkinsons?
Pill rolling resting tremor Cogwheel rigidity Loss of postural reflexes --> falls Bradykinesia
32
Exposure to what two toxins can lead to parkinsonian motor disorders?
Manganese CO ...also dopamine antagonists like Haloperidol
33
Where are Lewy bodies found in Parkinson's? What are Lewy bodies?
Intraneuronal Intracytoplasmic inclusions Lewy bodies are an accumulation of alpha-synuclein
34
WHat is the drug therapy for Parkinson's?
L-dopa Administer with Carbidopa, COMT and MAO-B inhibitors to prevent peripheral metabolism, and central breakdown of dopamine
35
What is the genetic basis for Huntington's Disease
CAG trinucleotide repeat of huntingtin gene on chromosome 4
36
What is the best treatment for Huntington's Disease?
Dopamine antagonists- to lessen hyperkinesia, choreoathetosis and behavior problems
37
What are surgical treatment options available for PD?
PD is due to over inhibition of the thalamus by the GPm. Pallidotamy --> destructive stereotactic lesions of the GPm to lessen inhibition of thalamus You can also inhibit the STN, which then shuts down the inhibitory indirect pathway of the basal ganglia
38
Alzheimer's affects what part of the brain?
The cerebral cortex
39
How prevalent is alzheimer's disease?
It is the most common cause of senile dementia in people over the age of 65
40
Describe the genetics of familial alzheimer's (10% of all AD)
Amyloid precursor protein (APP) on chromosome 21 Presenilin 1- chromosome 14 Presenilin 2- chromosome 1 They all increase the production of A-Beta peptide production, the major component of senile plaques
41
WHat is the role of ApoE in AD?
ApoE4 - increases chances of getting AD | ApoE2- protective against AD
42
What is the composition of neurofibrillary tangles of AD? What is the stain used to visualize it?
hyperphosphorylated tau proteins Visualized using Bielschowsky silver stain
43
How are amyloid senile plaques visualized/
Bielschowsky silver stain
44
Amyloid angiopathy is associated with what disease process?
AD -made of the same amyloid as the senile plaques
45
Lewy Body disease primarily affects what part of the CNS?
The cerebral cortex
46
What are the clinical features of Lewy Body dementia?
Dementia with visual hallucinations followed by parkinsonian symptoms Alpha-synuclein problem,
47
What is frontotemporal lobar degeneration?
Cerebral cortex degeneration in the frontal and temporal lobes. --> Changes in personal and social conduct, often associated with disinhibition and language changes
48
What type of disease is frontotemporal lobar degeneration?
Tauopathy
49
What is Pick's disease? What is the unique clinical feature?
Type of frontotemporal lobar degenerative dementia. Patients present with aphasia rather than memory loss, but go on to have dementia later on
50
What do Pick bodies look like, and what are they composed of?
Pick bodies are GLOBOSE, cytoplasmic inclusions. (very circular) They are composed of tau
51
Dementia is associated with what intracellular inclusions?
Lewy bodies- composed of alpha-synuclein
52
What two neurotransmitters are decreased (from the caudate) in Huntington's Disease?
ACh and GABA
53
What causes neuronal death in Huntington's ?
Over activation of NMDA-R by glutamate
54
What are the symptoms of multiple system atrophy?
Variable combination of parkinsonism, cerebellar ataxia, and autonomic dysfunction- depends on the neuronal system involved
55
WHat is the pathology of multiple system atrophy?
Glial cytoplasmic inclusions composed of alpha-synuclein
56
What is the gene associated with familial ALS?
SOD-1 (superoxide dismutase)
57
What is the gene associated with Werdnig-Hoffman syndrome?
SMN genes - survival of motor neuron genes
58
What is the genetic problem in frederich's ataxia?
AR, trinucleotide repeat of GAA, glutamic acid, of the frataxin gene located on chromosome 9 Frataxin is essential for mitochondrial iron regulation
59
What are the symptoms of Frederich's Ataxia?
Degeneration of the cerebellum--> ataxia Degeneration of the spinal cord tracts --> loss of DC, CST, and loss of deep tendon reflexses People die of cardiac causes
60
What is mixed dementia?
Alzheimer's disease + vascular dementia
61
What is CADASIL?
The most common form of vascular dementia. Involves small arterioles and capillaries
62
Wernicke's encephalopathy has what triad of symptoms?
Opthalmoplegia/nystagmus Cerebellar dysfunction Altered mental status
63
What is the appearance of the mammillary bodies in Wernicke's encephalopathy?
Petechial hemorrhaging
64
What structure in the brain is primarily affected by methanol?
Putamen
65
What structure is primarily affected by CO?
Globus pallidus
66
Name two other disease processes that closely mimic Subacute combined degeneration.
HIV- includes lots of other problems obviously Frederich's Ataxia: includes cerebellar dysfunction
67
What is the extrapyramidal system for?
Postural control
68
Patients with a positive Romberg sign have a defect where?
Dorsal column pathway
69
Patients who can't stand with their eyes open have a defect where?
Cerebellum
70
What is an ataxic gate? WHat causes it?
Wide-legged walk Patients with dorsal column degeneration, cerebellar degeneration, posterior column degeneration
71
What is the hemiplegic gait?
Stroke patient
72
What is a tabetic gait?
"Foot slapping" due to tabes dorsalis/destruction of dorsal column pathway
73
Waddling gait?
Myopathy
74
Scissors gait?
Cerebral palsy, multiple sclerosis , corticospinal tract lesion affecting legs. Unopposed adductors.
75
What causes hemiballismus?
Lesion (usually infarction) of the contralateral subthalamic nucleus
76
Speech is controlled by UMN, and modulated by what two structures?
Cerebellum and extrapyramidal systems
77
Epigastric aura's are a buzzword for what type of seizures?
Temporal lobe
78
What are characteristics of temporal lobe seizures?
most common partial seizures Characterized by staring, unresponsiveness, oroalimentary and gestural automatism
79
What precipitates a juvenile myoclonic seizure? How is it treated?
Alcohol use and sleep deprivation Treat with valproic acid
80
What are myoclonic seizurse?
Partial seizure with lightening "shivers"- happens throughout the morning/day

MHD- Neuro (19 decks)

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