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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
Q

How does Parkinson’s disease lead to a hypokinesia?

A

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

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26
Q

What causes hyperkinesia with hemiballismus?

A

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

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27
Q

How does Huntington’s disease lead to hyperkinesia?

A

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

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28
Q

Infarcts, hemorrhages, or tumors of the striatum or STN leads to what movement disorders?

A

Contralateral choreoathetosis or hemiballismus

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29
Q

Dopamine agonists lead to what types of movement disorders?

A

Hyperkinesia: chorea or dystonia

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30
Q

What generally causes asterixis?

A

Metabolic disorders

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31
Q

What are the 4 motor disturbances in parkinsons?

A

Pill rolling resting tremor
Cogwheel rigidity
Loss of postural reflexes –> falls
Bradykinesia

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32
Q

Exposure to what two toxins can lead to parkinsonian motor disorders?

A

Manganese
CO

…also dopamine antagonists like Haloperidol

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33
Q

Where are Lewy bodies found in Parkinson’s? What are Lewy bodies?

A

Intraneuronal Intracytoplasmic inclusions

Lewy bodies are an accumulation of alpha-synuclein

34
Q

WHat is the drug therapy for Parkinson’s?

A

L-dopa

Administer with Carbidopa, COMT and MAO-B inhibitors to prevent peripheral metabolism, and central breakdown of dopamine

35
Q

What is the genetic basis for Huntington’s Disease

A

CAG trinucleotide repeat of huntingtin gene on chromosome 4

36
Q

What is the best treatment for Huntington’s Disease?

A

Dopamine antagonists- to lessen hyperkinesia, choreoathetosis and behavior problems

37
Q

What are surgical treatment options available for PD?

A

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
Q

Alzheimer’s affects what part of the brain?

A

The cerebral cortex

39
Q

How prevalent is alzheimer’s disease?

A

It is the most common cause of senile dementia in people over the age of 65

40
Q

Describe the genetics of familial alzheimer’s (10% of all AD)

A

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
Q

WHat is the role of ApoE in AD?

A

ApoE4 - increases chances of getting AD

ApoE2- protective against AD

42
Q

What is the composition of neurofibrillary tangles of AD? What is the stain used to visualize it?

A

hyperphosphorylated tau proteins

Visualized using Bielschowsky silver stain

43
Q

How are amyloid senile plaques visualized/

A

Bielschowsky silver stain

44
Q

Amyloid angiopathy is associated with what disease process?

A

AD

-made of the same amyloid as the senile plaques

45
Q

Lewy Body disease primarily affects what part of the CNS?

A

The cerebral cortex

46
Q

What are the clinical features of Lewy Body dementia?

A

Dementia with visual hallucinations followed by parkinsonian symptoms

Alpha-synuclein problem,

47
Q

What is frontotemporal lobar degeneration?

A

Cerebral cortex degeneration in the frontal and temporal lobes.

–> Changes in personal and social conduct, often associated with disinhibition and language changes

48
Q

What type of disease is frontotemporal lobar degeneration?

A

Tauopathy

49
Q

What is Pick’s disease? What is the unique clinical feature?

A

Type of frontotemporal lobar degenerative dementia.

Patients present with aphasia rather than memory loss, but go on to have dementia later on

50
Q

What do Pick bodies look like, and what are they composed of?

A

Pick bodies are GLOBOSE, cytoplasmic inclusions.
(very circular)

They are composed of tau

51
Q

Dementia is associated with what intracellular inclusions?

A

Lewy bodies- composed of alpha-synuclein

52
Q

What two neurotransmitters are decreased (from the caudate) in Huntington’s Disease?

A

ACh and GABA

53
Q

What causes neuronal death in Huntington’s ?

A

Over activation of NMDA-R by glutamate

54
Q

What are the symptoms of multiple system atrophy?

A

Variable combination of parkinsonism, cerebellar ataxia, and autonomic dysfunction- depends on the neuronal system involved

55
Q

WHat is the pathology of multiple system atrophy?

A

Glial cytoplasmic inclusions composed of alpha-synuclein

56
Q

What is the gene associated with familial ALS?

A

SOD-1 (superoxide dismutase)

57
Q

What is the gene associated with Werdnig-Hoffman syndrome?

A

SMN genes - survival of motor neuron genes

58
Q

What is the genetic problem in frederich’s ataxia?

A

AR, trinucleotide repeat of GAA, glutamic acid, of the frataxin gene located on chromosome 9

Frataxin is essential for mitochondrial iron regulation

59
Q

What are the symptoms of Frederich’s Ataxia?

A

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
Q

What is mixed dementia?

A

Alzheimer’s disease + vascular dementia

61
Q

What is CADASIL?

A

The most common form of vascular dementia. Involves small arterioles and capillaries

62
Q

Wernicke’s encephalopathy has what triad of symptoms?

A

Opthalmoplegia/nystagmus
Cerebellar dysfunction
Altered mental status

63
Q

What is the appearance of the mammillary bodies in Wernicke’s encephalopathy?

A

Petechial hemorrhaging

64
Q

What structure in the brain is primarily affected by methanol?

A

Putamen

65
Q

What structure is primarily affected by CO?

A

Globus pallidus

66
Q

Name two other disease processes that closely mimic Subacute combined degeneration.

A

HIV- includes lots of other problems obviously

Frederich’s Ataxia: includes cerebellar dysfunction

67
Q

What is the extrapyramidal system for?

A

Postural control

68
Q

Patients with a positive Romberg sign have a defect where?

A

Dorsal column pathway

69
Q

Patients who can’t stand with their eyes open have a defect where?

A

Cerebellum

70
Q

What is an ataxic gate? WHat causes it?

A

Wide-legged walk

Patients with dorsal column degeneration, cerebellar degeneration, posterior column degeneration

71
Q

What is the hemiplegic gait?

A

Stroke patient

72
Q

What is a tabetic gait?

A

“Foot slapping” due to tabes dorsalis/destruction of dorsal column pathway

73
Q

Waddling gait?

A

Myopathy

74
Q

Scissors gait?

A

Cerebral palsy, multiple sclerosis , corticospinal tract lesion affecting legs. Unopposed adductors.

75
Q

What causes hemiballismus?

A

Lesion (usually infarction) of the contralateral subthalamic nucleus

76
Q

Speech is controlled by UMN, and modulated by what two structures?

A

Cerebellum and extrapyramidal systems

77
Q

Epigastric aura’s are a buzzword for what type of seizures?

A

Temporal lobe

78
Q

What are characteristics of temporal lobe seizures?

A

most common partial seizures

Characterized by staring, unresponsiveness, oroalimentary and gestural automatism

79
Q

What precipitates a juvenile myoclonic seizure? How is it treated?

A

Alcohol use and sleep deprivation

Treat with valproic acid

80
Q

What are myoclonic seizurse?

A

Partial seizure with lightening “shivers”- happens throughout the morning/day

MHD- Neuro (19 decks)

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