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BIOL 350: Clinical Neuroscience > Final Exam Practice Questions > Flashcards

Final Exam Practice Questions Flashcards

1
Q

A 70-year-old woman presents with dysarthria and motor hemiparesis. Her medical history includes type 2 diabetes mellitus and hypertension. The imaging study revealed an ischemic stroke involving the left frontal lobe. The medical plan would be to give her medication to relieve the clot obstruction. Based on the next possible answers, which is an absolute contraindication for the recommended therapy?

Decompression skull surgery 9 months before

The history of retinal coagulopathy treated with photocoagulation

The symptoms onset < 3h

Systolic blood pressure > 200 mmHg

A

Systolic blood pressure > 200 mmHg

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2
Q

A 70-year-old woman presents with dysarthria and motor hemiparesis. Her medical history includes type 2 diabetes mellitus and hypertension. The imaging study revealed an ischemic stroke involving the left frontal lobe. The medical plan would be to give her medication to relieve the clot obstruction.

Following the same clinical case study, what was the recommended treatment?

tPA

Antiplatelet drug

Thrombectomy

Aspirin

A

tPA

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2
Q

A 70-year-old woman presents with dysarthria and motor hemiparesis. Her medical history includes type 2 diabetes mellitus and hypertension. The imaging study revealed an ischemic stroke involving the left frontal lobe. The medical plan would be to give her medication to relieve the clot obstruction.

Before administering the treatment for the same patient, what imaging study should be obtained?

MRI of the brain with gadolinium contrast

NCCT of the head

Contrast CT of the head

X-rays of the skull

A

NCCT of the head

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3
Q

A 70-year-old woman presents with dysarthria and motor hemiparesis. Her medical history includes type 2 diabetes mellitus and hypertension. The imaging study revealed an ischemic stroke involving the left frontal lobe. The medical plan would be to give her medication to relieve the clot obstruction.

The patient had a good recovery after hours of drug administration. Then, suddenly, the patient’s initial symptoms worsened. Also, new symptoms appeared such as confusion, low blood pressure, and headache. Based on the history of this patient what do you think should be the next step to do?

Head MRI

Cerebral ultrasound

Head NCCT

Brain X-ray

A

Head NCCT

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4
Q

The patient had a good recovery after hours of drug administration. Then, suddenly, the patient’s initial symptoms worsened. Also, new symptoms appeared such as confusion, low blood pressure, and headache. What do you think that happened in the previous clinical case after the drug administration?

Adverse event of the drug is suspected, intracranial bleeding should be suspected

Nothing, this is an expected symptom curve when we talk about ischemic strokes. The patient should recovered and only monitoring is recommended

The ischemic stroke worsened and another site of a possible ischemic stroke could be found

The penumbra area failed to recovered after treatment and nothing should be done

A

Adverse event of the drug is suspected, intracranial bleeding should be suspected

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5
Q

What is the first test that should be performed when a patient is present in the emergency room with symptoms of a stroke?

Complete blod count with fibrinogen measure to evaluate blood clotting

Brain CT scan

Brain MRI

Electrocardiogram to see if the heart is not a possible cause of embolism

A

Brain CT scan

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6
Q

A 45-year-old male presents to the emergency department with a sudden onset of neurological symptoms such as dysarthria, mild weakness in his right arm, and low weakness in the right leg. The medical history of this patient is that she had a clotting disease 15 hours ago and was treated with anticoagulants. The NIHSS score is 8 in the physical examination. What would be the first imaging study you would suggest?

NCCT of the head
MRI of the head
MRI angiography
Contrast enhanced CT scan

A

NCCT of the head

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7
Q

A 45-year-old male presents to the emergency department with a sudden onset of neurological symptoms such as dysarthria, mild weakness in his right arm, and low weakness in the right leg. The medical history of this patient is that she had a clotting disease 15 hours ago and was treated with anticoagulants. The NIHSS score is 8 in the physical examination. There is no changes in the imaging study you suggested. What study would you suggest to perform after 3 hours of onset of symptoms?

MRI of the head
Ultrasound of the head
CT scan of the head
X-ray of the skull

A

MRI of the head

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8
Q

A 45-year-old male presents to the emergency department with a sudden onset of neurological symptoms such as dysarthria, mild weakness in his right arm, and low weakness in the right leg. The medical history of this patient is that she had a clotting disease 15 hours ago and was treated with anticoagulants. The NIHSS score is 8 in the physical examination. What artery’s territory would you say is affected in this patient based on the syndrome’s characteristics presented?

Middle cerebral artery territory
Posterior cerebral artery territory
Vertebrobasilar territory
Anterior cerebral artery territory

A

Middle cerebral artery territory

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9
Q

A 72-year-old female is brought to the hospital by EMS after being found unresponsive at home. On arrival, she is noted to have a Glasgow Coma Scale (GCS) score of 10, right-sided facial droop, and right-sided hemiparesis. Additionally, she is unable to follow commands or speak. Bilateral hemianopia. During the neurological assessment, she demonstrates severe dysarthria and no movement of the right side of her body. What could be a close NIHSS score for this patient?

10
35
15
5

A

35

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10
Q

What is the primary symptom of Parkinson’s disease?

Postural instability
Rigidity
Resting tremor
Bradykinesia

A

Bradykinesia

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11
Q

Which of the following is not a characteristic feature of Parkinson’s disease?

Excessive appetite
Sialorrhea
Mood disorders
REM sleep disorder

A

Excessive appetite

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12
Q

What is the estimated prevalence of Parkinson’s disease in individuals above 60 years of age?

2% to 3%
1% to 2%
Less than 1%
More than 3%

A

1% to 2%

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13
Q

Parkinson’s disease is primarily associated with the loss of which type of neurons in the substantia nigra?

Cholinergic neurons
Carbadopaminergic neurons
GABAergic neurons
Dopaminergic neurons

A

Dopaminergic neurons

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14
Q

Which environmental factor has been linked to an increased risk of Parkinson’s disease?

Exposure to pesticides and herbicides
Regular exercise
Consumption of green leafy vegetables
Adequate sunlight exposure

A

Exposure to pesticides and herbicides

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15
Q

What is the major component found in Lewy bodies, a characteristic histopathological feature of Parkinson’s disease?

Glial fibrillary acidic protein
Beta-amyloid protein
Tau protein
Alpha-synuclein

A

Alpha-synuclein

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16
Q

According to the proposed staging scheme by Braak and colleagues, which brain region is affected earliest in Parkinson’s disease?

Basal forebrain
Locus ceruleus
Dorsal motor nucleus of the vagus
Substantia nigra

A

Dorsal motor nucleus of the vagus

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17
Q

Which of the following is not considered a prominent feature of Parkinson’s disease in the clinical examination?

Slowness (bradykinesia)
Gait disturbance
Cerebellar dysfunction (loss of coordination)
Tremor

A

Cerebellar dysfunction (loss of coordination)

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18
Q

Pharmacologically, which medication is typically used in the treatment of Parkinson’s disease to improve CNS bioavailability of levodopa?

Carbidopa
Pramipexole
Amantadine
Selegiline

A

Carbidopa

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19
Q

What treatment approach is increasingly used for advanced Parkinson’s disease patients who do not respond well to medication?

Transcranial magnetic stimulation
Electroconvulsive therapy
Cognitive behavioral therapy
Deep brain stimulation

A

Deep brain stimulation

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20
Q

A 68-year-old male presents to the clinic with a complaint of tremors in his right hand that worsen at rest but improve with intentional movements. He also reports a gradual onset of slowness in movement and stiffness in his limbs. Which of the following symptoms is most suggestive of Parkinson’s disease?

Resting tremor
Muscle weakness
Slowness in movement
Stiffness in his limbs

A

Slowness in movement

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21
Q

A 55-year-old female visits her physician with constipation, excessive drooling, and difficulty sleeping. Upon further evaluation, the patient is noted to have complaints of unilateral bradykinesia and rigidity on physical examination. The neurological evaluation reports moderate cognitive impairment. Which of the following conditions is most likely causing her symptoms?

Parkinsonism
Stroke
Parkinson’s disease
Alzheimer’s disease

A

Parkinson’s disease

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22
Q

A 70-year-old man presents with a history of gradually worsening gait disturbance characterized by shuffling steps, reduced arm swing, and difficulty with turning. He also reports a feeling of stiffness in his limbs, especially upon waking up in the morning. Which of the following features is most commonly associated with advanced Parkinson’s disease?

Excessive daytime sleepiness
Freezing of gait
Hypersalivation
Unresponsive face

A

Freezing of gait

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23
Q

What is the most common type of dementia, accounting for at least two-thirds of cases in people aged 65 and older?

Parkinson disease
Alzheimer’s disease
Vascular dementia
Lewy body dementia

A

Alzheimer’s disease

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24
Q

Which of the following symptoms is typically an early sign of Alzheimer’s disease?

Spatial delusions
Motor symptoms like tremors
Aggressiveness
Episodic short-term memory loss

A

Episodic short-term memory loss

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25
Q

What is the genetic role identified for both early and late-onset Alzheimer’s disease?

Mutations in the PSEN1 gene
Trisomy 18
Chromosome 14 abnormalities
Presence of APOE e4 allele

A

Presence of APOE e4 allele

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26
Q

Which of the following is NOT a risk factor associated with Alzheimer’s disease?

Family history of dementia
Increasing age
Traumatic head injury
Diet with high levels of beta amyloid

A

Diet with high levels of beta amyloid

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27
Q

What are the core histological features of Alzheimer’s disease?

Granulovacuolar degeneration only
Neurofibrillary tangles only
Both neurofibrillary tangles and plaques
Plaques only

A

Both neurofibrillary tangles and plaques

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28
Q

What is the most common cause of death in Alzheimer’s disease patients?

Cardiovascular disease
Stroke
Pneumonia
Cancer

A

Pneumonia

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29
Q

What percentage of patients with mild cognitive impairment progress to dementia per year?

10%
5%
20%
40%

A

10%

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30
Q

What is the average life expectancy for a person diagnosed with Alzheimer’s disease at age 65 or older?

1-2 years
20 years or more
10-15 years
4-8 years

A

4-8 years

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31
Q

What is a cerebrovascular disease?

A

A stroke or cardiovascular accident (CVA) that causes the blood supply to be cut off to an area of the CNS that causes irreversible affects to the tissues. But in the surrounding compromised tissues (penumbra) area may be salvageable.

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32
Q

What is the stroke warning? Acronym? What does it stand for? What part does each affect?

What is the motto?

A

B.E F.A.S.T

Balace loss (Cerebellum)
Eyesights (Temporal/Occipital lobe)
Face drooping (Brainstem)
Arm weakness (Frontal lobe)
Speech difficulty (Fontal lobe)
Time to call 911

TIME IS BRAIN!

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33
Q

What is the second most leading cause of death worldwide and a contributor in disabilities? (With a 1:1 ratio risk)

Alzheimer
Trauma
Stroke (cerebrovascular disease)
Multiple sclerosis

A

Stroke (cerebrovascular disease)

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34
Q

How many blood vessels supplies the Circle of Wilis and what are they called?

A

4 in total (Left and Right)
- Common carotid artery
- Vertebral artery

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35
Q

What are the different types of strokes and their different characteristics?

A

Ischemic Stroke: Blood clot in the brain that blocks blood flows leading to a reduce in blood supply causing cell death. Also considered to be the most common accounting for 65-84% of all strokes.

Hemorrhagic Stroke: Ruptures of the blood vessels leading to causing intracranial pressure. Aneurysm and AVMs are contributing causes. With uncontrolled high blood pressure being the most common cause.

Transient Ischemic attacks (TIA): a warning stroke that causes a temporary clot.

Cryptogenic stroke: Cause of stroke that cannot be determined

Brainstem stroke: Affects of both sides of the body leaving the individual in a lock-in state.

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36
Q

What is the common characteristics between an ischemic stroke and a hemorrhagic stroke?

A

Both cut oxygen rich blood supply to the tissues within the brain.

37
Q

What are the two different types of hemorrhagic strokes and explain how their different?

A

Intracerebral hemorrhage (ICH) is bleeding into functional tissues within the brain and Subarachnoid hemorrhage (SAH) is bleeding into the subarachnoid space on the brain.

38
Q

Risk factors of ischemic stroke generally and by TOAST?

A

Generally, risk factors such as age, smoking habits, and diseases such as cardiac and diabetes cause higher chances but there are many risk factors.

According to TOAST, the 3 primary cause is large vessel disease (inflammation and build up of lipids), small vessel disease (constriction of the artery), and cardioembolism (the heart pumping unwanted materials into the brain circulation).

39
Q

What are the general risk factors and specific risk factors for ICH and SAH?

A

Risk factors for both: age, drug use (stimulation of blood vessels), anticoagulants, hypertension, alcohol use, and smoking.

ICH: Rupture of small artery due to hypertension vasculopathy (any disease affecting blood vessels)

SAH: 85% of the time is cause by ruptured aneurysm or family history of aneurysm. Can also be aditionally caused by coagulopathy and AVMs.

40
Q

Steps to diagnosis a stroke?

A
  1. Primary clinical evaluation (Cincinnati Scale: testing the face, arm, and speech; 72% if 1/3 failed and more than 85% if 3/3 failed)
  2. Imaging and testings (NIHSS, blood pressure, and glucose testing)
  3. Evaluation of the cause

Patient’s history: Risk factors and medications would be helpful

41
Q

What is the NIHSS test?

A

The NIHSS is a 15 scale item to evaluate patient’s level of consciousness, language, motor, and sensory by asking patients to answer questions. This test is useful for choosing treatment and predicting outcomes.

42
Q

Clinical manifestation of Ischemic stroke:

Anterior cerebral artery (uncommon)
Middle cerebral artery (common)
Posterior cerebral artery
Vertebrobasilar system

A

Anterior cerebral artery: Affects in the legs
Middle cerebral artery: Affects the head and arms
Posterior cerebral artery: Affects vision
Vertebrobasilar system: Affects the brainstem and cranial nerves

43
Q

Clinical manifestation of ICH and SAH

A

Clinical manifestation of ICH is dependent on the location and size of the hemorrhage but typically causes nauseas, vomiting, and headaches. With seizures being more common. Blood pressure also increases due to a mechanism.

Clinical manifestation of SAH is described commonly as a sudden and intense headache considered to be the worst headache ever experienced.

44
Q

Clinical manifestation of TIA

A

Clinical manifestation will show symptoms of stroke for approximately 24 hours but will typically only last 1 hour.

ABCD2 test is done to see risk for a stroke in one week

45
Q

Imaging Diagnosis of Strokes

A

NCCT (non-contrast CT scans are ALWAYS the first imaging for all patients suspected of a stroke)

With lumbar puncture recommended for cases when CT scans yield a negative result.
With NCCT and MRI appropriate for excluding ICH before administering alteplase.

46
Q

Name the layers, space of the brain, and strokes associated with each layer.

A

Brain
(Epidural hemorrhage)
Dura Mater
(Subdural hemorrhage)
Arachnoid Mater
(Subarachnoid hemorrhage: Runs with CSF can occur in ventricles)
Pia Mater

47
Q

General treatment for strokes?

A

Maintain high blood pressure for ischemic areas in the brain
Maintain oxygen saturations
Maintain glucose levels

48
Q

Treatment of ischemic stroke

A

Patients with thrombi (stagnant clot) or emboli (clot movement from one place to another):

Alteplase (tPA) within 4 hours and a half of first symptoms onset
Thrombolysis-in-situ as a medicine injector to get rid of clot
Mechanical thrombectomy, a mechanical removal like surgery
Anticoagulant
Antiplatlets (only if tPA has not been given) and within 48 hours of symptoms onset

49
Q

Treatment of ICH and SAH

A

ICH is mainly supportive care with consulting for surgical evacuation (removal of clot/blood to remove pressure), with anticoagulant/antiplatelet prohibited

SAH is with bed rest/supportive care with treatment of symptoms such as headaches

50
Q

Hyperdense and Hypodense

A

Hyperdense: white ares in a scan, filled with blood and hemorrhage

Hypodense: darker areas in scan which is the open spots or fluid fill

51
Q

What is Acquired Brain Injury (ABI)

A

Any damage to the brain after brith that is not due to a birth defect, disability, or progressive brain damage. A person who was previously neurologically intact but acquired some brain pathology.

Tauma = ABI

52
Q

What stands as the foremost contributor of disability among people under 40 years old?

A

Traumatic Brain Injury (TBI) with it most likely to affect males

53
Q

What two incidents make up the most common traumatic brain injury? Which one is more common?

A

Car accidents 12-17% and Falls (more common) 35-42%

54
Q

What are the two mechanisms of injury?

A

Contusion: Bleeding or Bruising (ex: injury to scalp)

Rotational forces: Twisting and rotational force to brain (ex: diffuse axonal injury (DAI) or tearing of bridging veins)

55
Q

What are the two types of ABI?

A

Focal: In one location at a specific location

Diffuse Axonal Injury (DAI): Widespread damage affecting multiple brain regions and white tract matter

56
Q

List three widely used indicators of severity in acute TBI?

A
  1. The Glasgow Coma Scale (GCS) (best score within 24 hours of injury): Eye opening, Motor response, and verbal response
    Initial assessment
  2. Duration of unconsciousness
  3. Duration of posttraumatic amnesia (PTA)
57
Q

Traumatic Brain Injury Severity

A

Mild:
GCS: 13-15
LOC: <15 minutes
PTA: <1 hour

Moderate:
GCS: 9-12
LOC: < 6 hours
PTA: 1-24 hours

Severe:
GCS: 3-8
LOC: 6-48 hours
PTA: 1-7 days

Very Severe:
LOC: >48 hours
PTA: >7 days

58
Q

What are the signs of skull fractures?

A

Raccoon eyes, blood collection in the back of the ear (battle signs), blood collection in the middle cavity of the ear, CSF from nose and ears, and bump

59
Q

What are the two factors that is dependent on for arms and leg movement after spinal cord injury?

A

The severity of the injury and the location of the injury

With bad severity possibly leading to a complete (all below the injury is lost), quadriplegia

Incomplete (some feeling and control of movement remains below the affected area, paraplegia

60
Q

What is Dementia and Alzheimer Disease, how are they related?

A

Dementia is a general term that encompasses a broad range of cognitive impairments.

Alzheimer Disease is a specific neurodegenerative condition that specifically affects 65 and older individuals.

Alzheimer is a type of Dementia and is the most common form.

61
Q

Alzheimer’s disease is gradual and __________ neurodegenerative disease caused by ____ ____ death. Typically starting in the _______ ________ in the ___________. In this cortex, a regularly spaced shaped grid pattern fire signals known as _______ ________, which sends out ______ signals.

A

progressive
neuronal cell
entorhinal cortex
hippocampus
grid cells
spatial

62
Q

_____ ______ plays a crucial role in the brain’s representation of space and ___________. Providing a framework for accurately ____________ and remembering ___________ ____________.

A

Grid cells
navigation
navigate
spatial location

63
Q

What are the four main risk factors of Alzheimer and some protective factors?

A

4 Risk Factors: Depression, Age, High parental age (associated with APP on chromosome 21), and APOE e4 allele (less effective at AB protein clearance leading to plague build up)

Protective Factors: Higher education, musical instruments/reading, healthy diet, and exercise

64
Q

Alzheimer can be inherited as an autosomal dominant disease by mutations of genes. Which proteins associated with what genes?

A

APP chromosome 21
PSEN1 chromosome 14
PSEN2 chromosome 1

65
Q

Alzheimer is characterized by the accumulation of two things, what are they and why do they cause the condition?

A

Plagues are a lesion formed due to elevations in Beta-Amyloid 42, with the formation of plagues being made of axonal ends and Beta-Amyloid made from cleavage of Amyloid precursor protein (APP)

Tangles are made up of Tau proteins that originally supports microtubules structure but once Beta-Amyloid is aggregated, the Tau protein hyperphosphorylate and cause aggregation leading to tangles starting in the hippocampus.

Tangles are thought to be more linked to Alzheimer than plagues.

66
Q

Stages of Alzheimer?

A

Pre-clinical or Asymptomatic
Mild cognitive impairment
Dementia stage (Issues with day to day task)

67
Q

Diagnosis of Alzheimer?

A

CT scans will show degeneration and widened third ventricle
MRI will show shrinkage of the brain, specifically medial temporal lobe
CSF testing for decrease in Beta-Amyloid 42 and increase of tau protein
The most important test is neuropsychological exam

Certainty of Alzheimer comes from post mortem biopsy

68
Q

What is Parkinson’s Disease

A

A neurodegenerative disease typically found in older individuals characterized by reduction in movement speed, bradykinesia (main symptom) and one additional characteristics such as tremor or muscle rigidity

69
Q

Epidemiology of Parkinson, what are the 5 mains point

A

Occurs more often in men than women
1-2 : 1000 people are affected
10% genetic deposition
Increase risk with age
Most cases are spontaneous

70
Q

What is the cause of Parkinson Disease?

A

PD impacts the basal ganglia and specifically, substantial nigra, with the issue lying in the loss of dopaminogeric neurons due to environmental stress (pesticide or industrial proximity) or oxygen radical

71
Q

What is the order in the direct pathway?

A

Cerebral cortex
+
Stratum
-
Globus Padillus (I)
-
Thalamus
+
Cerebral cortex

72
Q

What is the order in the indirect pathway?

A

Cerebral cortex
+
Stratum
-
Globus Padillus (E)
-
Subthalamic nucleus
+
Globus Padillus (I)
-
Thalamus
+
Cerebral cortex

73
Q

Nigrostriatal Pathway

A

Direct pathway depolarizes dopamine leading to excitation of the direct pathway causing more movement. Indirect pathway hyperpolarize dopamine leading to inhibition of the indirect pathway causing more movement.

This pathway excites the direct pathway and inhibits the indirect pathway leading to increase movement.

Therefore with decrease in dopamine, movement also decreases.

74
Q

Pathophysiology of Parkinson’s Disease, what is the alternative theory?

A

Alpha-synuclein a brain protein involved in neurotransmitter regulation in SNARE. With over accumulation of this alpha-synuclein in the brain, primarily substantial nigra causing formation of Lewy body or plagues that causes neuron degeneration which leads to loss of dopamine in the basal ganglia.

This accumulation can be caused by genetic mutation of PARK1 or environmental agent

There has been theories that PD appears in the myenteric plexus on the GIT and progresses up to involve dorsal motor nucleus, vagus nerves, pons, and midbrain.

75
Q

What are the different stages of Parkinson’s Disease?

A

Braak 1/2: Dorsal motor nucleus of the vagus and olfactory are affected with olfactory and autonomic disturbances

Braak 3/4: Pons and substantial nigra are affected causing sleep and motor disturbances

Braak 5/6: Basal forebrain, medial temporal lobe, and amygdala is affected causing emotion and cognitive disturbances

76
Q

Main symptoms of Parkinson Disease and other general symptoms

A

Main Trait: Slow movement (bradykinesia), muscle rigidity, tremor, and gait disturbances (any disruption of ability to walk)

General: mood disorder, constipation, sleep disorder, drooling, depression, and anosmia (Loss of smell)

77
Q

Diagnosing of Parkinson’s Disease

A

History and physical examination
Unified Parkinson Disease Rating Scale can be utilized to test but Parkinsonism and neurodegenerative disorders must be excluded first.

There is no lab or test specifically for this disease

78
Q

Treatment of Parkinson’s Disease?

A

Levodopa and Carbidopa are use together, as Levodopa is a precursor of dopamine while carbidopa blocks conversion of levodopa into dopamine outside of the CNS as it is unable to past through the blood brain barrier, this allows for an INC levodopa transformation into dopamine in the CNS.

Deep Brain Stimulation (DBS) is preferred over surgical options with it stimulating sub thalamic nucleus, globus padillus, and thalamus/

79
Q

What Brain Structure does Huntington’s Disease, Alzheimer’s Disease, and Parkinson’s Disease affect and what kind of impairment does it cause?

A

Huntington’s Disease: Affects the Basal Ganglia, specifically, caudate and putamen leading to increase in movement effects

Alzheimer’s Disease: Affects the medial temporal lobe (hippocampus) causing spatial memory loss and issues with short term memory

Parkinson’s Disease: Affects the Basal Ganglia, specifically, substantial nigra causing decrease in movement

80
Q

What is Huntington’s Disease?

A

An autosomal dominant neurodegenerative condition that causes choreatic (irregular muscle movement) movements along with behaviour/cognitive issues

81
Q

What is the etiology of Huntington’s Disease?

A

HD is caused by an autosomal dominant mutation of the CAG trinucleotide repetition on the HTT gene. The elongated polygluatmate sequence (CAG) in the TT gene causes neurodegeneration and protein aggregation

With CAG repeat length longer than 35-55 repeats being a significant factor and can determine severity/onset

82
Q

What is cholera (dyskinesia), dystonia, and akinesia? What are they caused by?

A

Cholera Dyskinesia: General involuntary muscle movement. Caused by a loss in the enkephalin (neurotransmitter) containing medium spiny neurons (GABAergic inhibitory cells) in the indirect pathway.

Dystonia: Muscle tone and contraction
Akinesia: No movement
Both are caused by loss of substance P (neuropeptide neurotransmitter) containing neurons in the direct pathway

83
Q

There are multiple theories in the pathogenesis of HD, and more than one process can occur at the same time, what are the 5 different theories:

A
  1. Neuronal aggregation: accumulation of the HTT gene can cause impairment of the ubiquitin-proteasome pathway
  2. Transcriptional dysnfunction
  3. Excititoxicity (central nueron death): increase in glutamate or glutamate agonist
  4. Mitochondria dysfunction and metabolism changes
  5. Changes in the axonal transport and synaptic dysnfunction

Changes caused by neuronal death in the caudate, putamen, and cerebral cortex

84
Q

Clinical Manifestation of Huntington’s Disease?

A

Motor Disturbances: Start at the distal extremities (hyperkinetic and involuntary chorea) and spreads to proximal and axial location progressively. Chorea movement such as dystonia, hypokinesia, akinesia.

Behaviour and psychiatric issues: Onset starts even before motor disturbances and can cause issues like irritability, impulsivity, and depression

Cognitive dysfunction: Decline in executive functions but memory remains intact

Behaviour and cognitive dysfunction shows phenotype based on the region-specific location of neuronal death in the basal ganglia and cerebral cortex

85
Q

Diagnosis, Treatment, and Clinical course for Huntington’s Disease?

A

Diagnosis: Genetic Testing confirmation, lab and imaging test helps rule out syndromes

Treatment: focuses on syndrome management (dopamine depletion or dopamine receptor antagonists)

Clinical Course: pre symptomatic, prodromal, and manifestation. With 15-18 years survival after onset. With CAG repeats longer than 40 being associated with the disease, 36-40 showing a slower onset.

86
Q

What is multiple sclerosis?

A

MS is a chronic autoimmune CNS disorder that causes chronic inflammation, loss of neuronal cells, gloss, and demylienation. A replacement of healthy tissues with fibres tissues.

87
Q

Epidemiology of Multiple sclerosis 5 points?

A

Three times more prevalent in females than male
Onset typically between 20-40 years old, but can occur at any age
10% of cases are under 18 years old
Higher risk identified with location in the higher latitude North America and Europe contributed to genetic and environmental factors
Migration effects: where people move to these susceptible location during childhood can lead to increase risk

88
Q

The 3 main Etiology of Multiple Sclerosis?

A

Immune: associated with the inside out and outside in mechanisms where cross reactivity/inflammatory mediated tissue damage is inflicted through CD4+ T cells

Environmental: Latitude location, vitamin D deficiency, and EBV infection

Genetic: those related to someone with MS are at a 35-75% higher risk. Association with the HLA (human lymphocyte antigen) shows a higher correlation with MS

89
Q

What are two primary mechanism MS affects the CNS and the three effects that allow these mechanisms?

A

Inflammation (results in plagues formation/BBB injury) and neurodegeneration

Plaques result from focal inflammation causes myelin loss, edema, and axonal injury.

Microscopically MS lesions show mononuclear infiltrate and surrounding white matter infiltration.

Monocytes, macrophages, and microglia contribute to BBB disruption and systemic immune cell entry

90
Q

What are the 4 main classification of MS and the 3 categories that sometimes included in the MS spectrum?

A

Relapsing remittance (RR): the most common, new or old symptoms can occur for 24-48 hours and usually subside, but residuals symptoms accumulate over time leading to disability

Primary progressive (PP): a progressive disability worsening from onset of symptoms with no attacks

Secondary progressive (SP): after 10-15 years in RR, with gradual symptoms worsening with or without relapses

Progressive relapsing (PR): decline with superimposed attacks

Clinically isolated syndrome (CIS): single episode of inflammatory CNS demyelination

Fulminant: Severe MS with multiple relapses and rapid progression

Benign: overall mild disability with relapses being rare

91
Q
A

BIOL 350: Clinical Neuroscience (2 decks)

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