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Flashcards in Neuropathology 1 Deck (192)
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A: How should you initially examine an Unresponsive pt (4)

B: Describe the PUPIL testing (5)

A: Examine [Brain Stem Reflexes] (ME then PB Motor vs. Breathing vs. Pupils vs. Eye mvmnt)

Pupils testing

1. Pupil Dilation (hypothalamus-->brain stem-->spinal cord--> sympathetic ganglia)

2. Pupil Constriction (Oculomotor CN3 & Parasympathetics)

3. Pupillary Light Reflex (Doesn't rule out Metabolic Coma)

4. Small Pupils ([Narcotics/Glaucoma Cholinergic Eyedrops] vs. [Normal in Awake Elderly]

5. [Unilateral Large Pupil] (possible Oculomotor CN3 compression from uncal herniation) = EMERGENCY!!!


A: How should you initially examine an Unresponsive pt (4)

B: Describe the BREATHING testing (3)

A: Examine [Brain Stem Reflexes] (ME then PB Motor vs. Breathing vs. Pupils vs. Eye mvmnt)

Breathing testing

1. Cheyne-Stokesalternating tachypnea & apnea from bilateral cortical lesions vs. HF vs. sleeping elderly

2. Hyperventilation = mostly from pulmonary congestion

3. [Irregular Ataxic] = Lesion at/near [medullary cardiopulmonary control] --> impending respiratory failure


Emergent Evaluation of a Comatose pt should include what 4 Steps

1st: ABC = Airway / Breathing / Circulation

2nd: Check Blood-glucose --> Give [50% IV Dextrose] if necessary

3rd: W/u for Toxi-metabolic coma (don't forget CO poisoning and hypOthermia) - Myoclonic Jerks & Asterixis

4th: W/u for Structural Coma (hemorrhage / tumor / infarct) = hemispheric abnormalities


A: Describe the Persistent Vegetative State

B: Are Cranial Nerve Reflexes still intact? 

C: In a Vegetative State, which neural structures are still intact? (2)

D: What does this progress from?

Pt is Arousable but not really responsive

A: [Days-weeks post Cerebral Cortex anoxia] pt may appear awake + [roving eyes] + [pain response] but still no real responsiveness = Persistent Vegetative State

B: Some CN reflexes may still be intact (Brainstem & Spinal Cord are still intact)

C: Brainstem & Spinal Cord

D: Coma --> Minimal Return


A: Describe the Demented pt

B: How do you approach Advanced Directives for these pts

C: What is their Nutritional Status (2)

A: Pt who is progressively becoming [unaware of problems] and [unable to understand/communicate], typically associated w/behavioral changes

B: Establish Directives early! (since family will eventually assume all decision-making)

C: [Olfactory Dysfunction] --> No Appetite, but pt will still have "basic need" to hydrate. Tx= [PEG-Percutaneous Endoscopic Gastrostomy] vs. feeding tube


A: The SCN [Suprachiasmatic Nucleus] is located Above _____ _______  and is used as our ___ ___  ____& ___  _____. It keeps us on a _______. This is 1 of the nucleus from the _____. 

B: What type of EXTERNAL input does the SCN receive? [3] 

C: What internal Output does it send out?  

D: Biologic Rhythms  by the SCN are not linked exclusively to the _____ and works together with ___ _____. Name the 4 Categories, describe their timing and give example

E: When does SCN secrete the MOST hormones? 

A: The SCN [Suprachiasmatic Nucleus] is located Above Optic Chiasm and is used as our endogenous "biological clock" & CIRCADIAN Pacemaker. It keeps us on a 24 hour cycle, turning some systems on/off. This is a nucleus of the HYPOTHALAMUS. 

B: Light (reason its near Optic Chiasm), Food & Temperature

C: Sleep-Wake 
D: Biologic Rhythms  by the SCN are not linked exclusively to the HIPPOCAMPUS. It works together with Environmental Cues. These are the 4 Categories: 

1. Ultradian = less than 24 hours -->Resp/HR

2. Circadian = 24 hours --->Corticosterone rhythm 

3. Infradian = More than 24 but less than 1 year-->menstrual cycles

4. Circannual= every year---> Hibernation 
E: Highest amount of SCN hormone secretion = When ur Sleep


A: Disconnection syndromes usually result from _______ matter damage interfering with ____  ___ or ___   ____

B1: Define Alexia

B2: Define Agraphia

B3: Lesions in [NON-Dominant Hemispheres of cortical language center] --> ____

C: AWA is usually caused by  _______ stroke to _______ Lobe. ___ ____ of this area is affected

A: Disconnection syndromes usually result from WHITE matter damage interfering with Corpus Callosum or ANT commissure. 


1. Alexia = impaired reading (visual cortex is disconnected from language center)

2. Agraphia= impaired writing (motor cortex for dominant hand is disconnected from language center)

3:[NON-Dominant Hemisphere lesions] in the [mirror image locations of cortical language center]--> Aprosody (inability to interpret the [TIP-Tone/Inflection/Pitch] of language)

C: [Alexia without Agraphia] is usually caused by PCA stroke to Occipital Lobe. Corpus Callosum of this area is affected--->Seeing object in L eye CAN'T be interpreted in the R brain like normal. 



A: HemiBallismus

B: HuntIngtons

C: Parkinsons

A: Lesion of [SubThalamic Nucleus] --> less Stimulation of [Globus Pallidus: internal] --> HYPERKinesia (specifically VIOLENT limb flinging)

B: HuntIngton's = [Auto Dominant Degeneration of ((I)ndirect Striatum) 2° to [Chromo 4 trinucleotide repeats]] "Hunter was way too excited

C: Parkinson's = [Degeneration of (Substantia Nigra:Compact) = Loss of All Dopamine] 

DDEM = Dopamine & [Direct Path] Enable Movement



A: [Chorea and Dystonia] are SE of Dopamine _____ [blockers vs. agonist]

B: Name 4 Movement Disorders that are unrelated to Basal Ganglia

C: Name the 5 components of the Basal Ganglia

A: A: [Chorea and Dystonia] are SE of Dopamine AGONIST


1. Essential Tremor

2. [Myoclonus vs. Asterixis (ToxiMetabolic etiology)] 

3. Dystonia

4. Tic

C: [Caudate / Putamen / [Globus Pallidus] / [Substantia Nigra] / [SubThalamic Nucleus]]


A: Primary Clinical Signs of Parkinsonism (4) 

B: Secondary Clinical Signs of Parkinsonism (3)

A: PARK ham

  1. [Pill Rolling Resting Tremor]
  2. [Rigidity Cogwheel] 
  3. BradyKinesia
  4. [AReflexia posturally] --> Fall


-hypOphonic speech

-Autonomic Dysfunction (constipation / bladder problems / orthostatic hypOtension)



A: Causes of Parkinsonism (4)

B: Age of onset

C: Dx (2)

D: Histology


1) Parkinson's Dz

2) [Rare Degenerative Disorders (progressive supranuclear palsy vs. multiple system atrophy)= NOT responsive to levodopa

3) [Dopamine Blocker (Haloperidol) SIDE EFFECTS

4) [Manganese vs. Carbon Monoxide Poisoning]

B: onset between 40-70 y/o

C: [ 2 or more Primary Clinical Signs --- typically worst on 1 side and progressive] + [Responds to Dopaminergic tx] 

D: Lewy Bodies = [alpha synuclein cytoplasmic accumulations tht are eosinophilic]


A: Parkinson's Dz Tx (5)

B: Describe the 3 aspects of Surgical tx specifically

"Eat a SALAD after you Park" 

1. [Levodopa (Dopamine Precursor)]

2. Amantidine (weakly stimulates Dopamine release)

3. Anticholinergics (WEAK effect)

4. [Dopamine Agonist Post synaptic] (Ropinirole vs. Pramipexole): Also has ability to [DEC Long term Dyskinesia if given as monotherapy]

5. Surgical tx

-Used in Pts refractory to meds

-Pallidotomy: Intential Destructive Lesion of the [Globus Pallidus:internal]

-SubThalamic nuc. inhibition with implanted electrode




A: What is Levodopa co-administered with and why?

B: Describe How Long Levodopa has an effect. What can be given to mitigate this? (2)

C: Side Effects (4)


Levodopa = Parkinson's Dz tx

A: Administered with Carbidopa (decarboxylase inhibitor), which prevents peripheral Levodopa catabolism before it has chance to enter brain

B: DEC over time since there will continue to be dopaminergic neuron death. [MAO-B and COMT-inhibitors] sustain effective Levodopa levels


[Hallucinations vs. Psychosis vs. Chorea vs. DysTonia]


Lewy Body Dementia

A: Statistics

B: Clinical Course (2)

C: Describe the Histology. What parts of the brain is it found in (2)? 

Lewy Body Dementia is the SECOND common type of neurodegenerative dementia

B: [Dementia + Visual Hallucinations] --> [Parkinsonian sx]

C:  [alpha synuclein cytoplasmic accumulations tht are eosinophilic] - found in Cortex & Brainstem


Frontotemporal Degeneration

A: Statistics

B: Clinical manifestation

C: Genetic Cause

D: Dx (3)

A:[Frontotemporal Degeneration] is the THIRD common type of neurodegenerative dementia BUT MAY BE CONCOMITANT WITH ALZHEIMER'S. Typically worst on Left. 

B: Change in personal/social conduct, associated with disinhibition and language changes

C: [Chromo 17 Tau gene mutation]

D: Immunohistochemistry against: [Tau vs. Ubiquitin vs. TDP43]


A: Categorize Pick's Dz

B: Clinical Presenation 

C: Histology

D: What 2 neural structures are associated

A: RARE SubType of [Frontotemporal Dementia]

B: Aphasia (minimal memory loss but may develop Dementia)

C: Pick Bodies = Globose neuronal cytoplasmic inclusions made of Tau

D: Hippocamps and Cortex


Huntington's Dz

A: Genetic Cause

B: What effect does Caudate nc. degeneration have? (2)

C: In this Dz, what actually causes Neuronal Death

A: HuntIngton's = [Auto Dominant Degeneration of ((I)ndirect Striatum) 2° to [Chromo 4 trinucleotide repeats]] "Hunter was way too excited

B: [Degeneration of Caudate nc.] --> [DEC GABA and ACh] 

C: [NMDA-R binding and Glutamate] 


 [Multiple System Atrophy]

A: onset

B: Sx (3)

C: Histology

A: 40-60  (Parkinson's Dz Onset = 40-70)

B: Atrophy of COPS

1. Parkinsonism -Substantia nigra atrophy

2. Cerebellar Ataxia - Cerebellar atrophy

3. Autonomic dysfunction -[Olivary nc./Pons atrophy]

C: [GLIAL alpha synuclein cytoplasmic accumulations tht's eosinophilic]


Friedreich's Ataxia

A: Statistics

B: Genetic Cause

C: Clinical Manifestation (3)

[FriedreiCH'S Ataxia]

A: Most common Hereditary Ataxia

B: [Auto recessive GAA Trinucleotide repeat in Chromo 9 Frataxin gene] Frataxin is needed for mitochondrial iron

C: [FriedreiCH'S Ataxia]

1. [Cerebellar Degeneration]--> Ataxia

2. Heart Abnormalities --> 50% of deaths! 

3.  [Spinal Cord Degeneration] --> [Loss of 2TVP] + [Muscle Weakness] + [Loss of Deep Tendon Reflex]


A: Mixed Dementia mostly consist of _____ & [Vascular Dementia]

B: What are Risk Factors for Mixed Dementia (2)

C: What is the most common form of [Vascular Dementia]

A: Mixed Dementia mostly consist of Alzheimer's & [Vascular Dementia]


1) [ApoE4 genotype] INC risk of Alzheimer's AND CV Dz

2) Vascular Amyloidosis INC risk of hemorrhagic strokes --> [Vascular Dementia]

C: CADASIL = involves small arterioles & capillaries


[Ethanol Tox: Wernicke's Syndrome]

A: Clinical Triad (3)

B: This syndrome is characterized by deficiency of what substance?

C: What supplement deficiency is this syndrome caused by?


A: Thiamine deficiency ---> 

1. Oculomotor abnormalities (ophthalmoplegia vs. nystagmus)

2. Cerebellar Dysfunction

3. Altered Mental Status

B: [+/- Korsakoff Psychosis from mammillary body hemorrhage & atrophy (can't recall recent memory so compensates with confabulation)] 

C: Thiamine Deficiency


A: Toxicity of what compound causes

[Cortical Atrophy] and [Central Pontine Myelinolysis]

B: [Central Pontine Myelinolysis] Histology

C: What Electrolyte abnormality causes [Central Pontine Myelinolysis] ?


B: Triangular lesion with myelin loss of the Pons

C: [Rapid Correction of Chronic hypOnatremia]


Methanol Toxicity 

A: MOD (3)

B: Clinical Manifestation (4)

A: Hepatic oxidation of [Methanol --> (Formaldehyde & Formic Acid)]-->

-global hypoxia

-white matter necrosis & hemorrhage--> [Putamen & Claustrum hemorrhagic infarct]

B: [Vision loss vs. Delirium/Convulsions vs. Coma vs. Death]


Gross Histology of Carbon Monoxide Toxicity (3)

  1. [Bilateral Globus Pallidus Hemorrhagic Necrosis]
  2. [White Matter Hemorrhagic Petechiae]
  3. Cerebral Edema


A: Identify and Describe Histology of image

B: Cause

A: [Alzheimer Type 2 Astrocyte] = [Nuclei are large and appear clear]

B: liver Failure--> Hyperammonemia (Hepatic Encephalopathy)



A: Speech consist of ____ and ____

B: Describe each component of Speech 

C: Define Aphasia

A: Speech = Phonation and Articulation

-Phonation: making sounds with vocal cord mvmnt (Vagus CN10) - (Dysphonia = Hoarse vs. whispery)

-Articulation: articulating sounds with [lips/tongue/palate/pharynx] (Dysarthria = slurred speech 2º to Articulation problems

B: Disorder of [previously acquired language ability] due to [language center lesion in dominant hemisphere] --> all-around impaired communication (includes gestures & Braille)


A: Where are the Cortical Language Centers

B: what perfuses this center

C: Describe the Function of Wernicke and Broca area

D: Lesions around this Center leads to what guaranteed defect? 

A: [Sylvian Lateral Sulcus] of the dominant (usually L hemisphere) hemisphere



1) Wernicke's area = language comprehension

2) Broca's area = language execution/expression

D: Imperfect Repetition 


A: Paraphasia definition

B: Examples (3)

[Word or Syllable Substitutions]

-Phonemic or literal = Sully for Silly

-[Semantic or verbal]= blue for Green

-Neologism= nonsense word: scatifang


Broca's Aphasia

A: Location of Lesion (2)

B: Clinical Manifestation (5)

A: [Area 44 Inferior Frontal Gyrus] + [involvement of adjacent motor cortex]


-[Poor Repetition/Naming/Fluency ([telegraphic nonfluency ( "I.....up.....early")]]

-R Hemiparesis

-Facial Weakness


Wernicke's Aphasia

A: Location of Lesion

B: Clinical Manifestation (4)

C: What Dx is this sometimes confused with?

A: [Temporal Lobe (posterior vs. superior)] 


-[Poor Repetition/Naming/Comprehension (They don't comprehend you and You can't comprehend them)]


C: Psychiatric disorders