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Describe the 2 Major Divisions of Cranial Venous Drainage -Superficial Veins (5) vs. Deep Veins (6)

****Superficial Veins*** 1. Superficial group = Dumps INto Superior/inferior Sagittal Sinuses 2. Inferior group= empties with transverse AND cavernous sinus ---->[SUP/inf sagittal sinus]----> **[SINUS CONFLUENCE]**---->Transverse sinuses--->IJV


Deep Veins = empty into [Internal cerebral Veins] --->[GREAT VEIN OF GALEN]----->Straight Sinus---->**[SINUS CONFLUENCE]**----->Transverse sinuses ------>IJV


What does the CT scan delineate? 

SubArachnoid Hemorrhage going into the Cisterns


A: What type of Nystagmus does Drugs/Metabolic produce? 

B: What type of Nystagmus does Anatomical lesions produce? 

C: Give an example of Physiological Nystagmus

A: Symmetrical Nystagmus

B: Asymmetrical nystagmus

C: Rotating in a swivel chair and then suddenly stopping


A: MOD for Bell's Palsy

B: Clinical Manifestation (3)

C: Cause

D: Short-term tx

A: BeLLs Palsy= Sudden and Non-traumatic Lesion of Facial LMN = complete face droop


[possible taste loss over ipsilateral ANT Tongue (chorda tympani branch)] 


[possible ipsilateral hyperacusis (stapedius branch)]

C: [Facial CN7 inflammation in petrous bone (possibly viral)]

D: Steroids


List Clinical Manifestation for these Facial CN7 lesions

1. [Facial CN7 LMN]

2a. [Petrous Bone: Chorda tympani fibers]

2B. [Petrous Bone: Stapedius fiber]

3. [CAAN- Cerebellopontine Angle Acoustic Neuroma]

4. [Pontine Lesion]


[Facial Paralysis ipsilateral / Taste loss / Sound sensitivity INC / Deafness&Tinnitus / Lateral Gaze impairement] 

1. [Facial CN7 LMN] = F 

2a. [Petrous Bone: Chorda tympani fibers] = FT

2B. [Petrous Bone: Stapedius fiber] = FTS

3. [CAAN- Cerebellopontine Angle Acoustic Neuroma] = FTSD

4. [Pontine Lesion] = FTSDL


Brain Stem Synromes


A: Brain stem lesions (2)

B: [R Pontine Infarct] (2)

A. Brain stem lesion -->

-ipsilateral CN deficit

-Contralateral UMN limb weakness

B: R Pontine Infarct-->

-[R LMN Facial Weakness from CN7 deficit]

- [L Hemiparesis from (Corticospinal Pyramidal tract) deficit] 


Stroke - Brain Stem Syndromes


 [Medial Midbrain of Weber syndrome]

A. [Medial Midbrain of Weber syndrome]

**Occlusion of [POST Cerebral a.] --> 

1. ipsilateral CN3 lesion

2. Contralateral hemiplegia (Cerebral Peduncle)



A: Explain the *Rinne Test* [3] 

B: What two Auditory Defects does it differentiate between?

1st: Place vibrating tuning fork on mastoid process of suspected side. Pt should hear vibrations in that ear = Bone conduction route intact 

2nd: While tuning fork is still vibrating move prongs of fork to [outside ear pinna]--> where Air conduction is 100x more sensitive than bone

3rd: Pt should still hear sound for 15 more seconds. If pt can't hear sound for that long = air conduction deafness on that side

B: Differentiates between [Air and SensoriNeural: 2nd step] defects


A: Explain **WEBER'S TEST** [4]

B: What two Auditory Defects does it differentiate between?

1st: Tuning Fork placed on Skull midline 

2nd: Normally sound is conducted simultaneously by both [ossicular air] and [bone] routes which are out of phase w/each other (1vibration up and 1vibration dwn)

3rd: Being out of phase--->Cancel each other out on both sides of head-->sound perceived as coming from midline

4th: If [ossicular air] route loses conduction, cancellation effect on tested ear is DEC and net vibration will be GREATER on the AFFECTED SIDE

can also be caused by [CTL Ear has SensoriNeural defect]

B: Differentiates between [Air and SensoriNeural defect: 1st step]


A: Clinical Course of Carbon Monoxide Poisoning

B: Tx 

C: Which drugs cause Drug-related Stroke Syndrome (4)

1st: HA / vomiting / blurred vision

2nd: Coma / Seizures / Cardiopulm arrest (Amnesia / Parkinsonism)

B: [Hyperbaric O2 chamber]

C: [Cocaine (most common) / Amphetamine / PCP / LSD]--> vasoconstriction or abrupt HTN-->cerebral infarct/hemorrhage


A: Describe the 2 stages of EtOH Withdrawal

B: What factors can be Fatal during EtOH Withdrawal (2)

C: When is a Brain Scan during EtOH Withdrawal warranted?

1. [Early Hypersympathetic Stage] = tremors + sweaty + tachycardia + [limited convulsive Tonic-->Clonic seizures] tht occur 12 hrs-3 days post drinking]

2. [Later (3-4 days post drinking) Delirium Tremen Stage] = [Fluctuating motor/autonomic activity] + confusion + hallucinations(visual and auditory)

B: Coexisting infectio vs. Trauma

C: If pt has [Partial / Focal Seizure] this suggest focal lesion


Chronic Alcoholism Syndrome

A: Causes (3)

B: What type of Head Trauma can it cause? (2)

C: Clinical Manifestations (4)


-EtOH itself

-Malnutrition from EtOH

-Vitamin (B1) Deficiencies from EtOh

B: [Subdural vs. Cerebral Hemorrhage] 


1. [Wernicke Encephalopathy] ---> [Korsakoff Psychosis]

2. [Alcoholic (ANT SUP Cerebellar vermis) Degeneration]

3. Peripheral Neuropathy

4. Dementia


Chronic Alcoholism Syndrome

A:  [Wernicke Encephalopathy] 

-Sx (4)


B: [Korsakoff Psychosis]

-Sx of [Korsakoff Psychosis]

A:  [Wernicke Encephalopathy] 

-[Nystagmus vs. Ophthalmoplegia vs. (Gait ataxia) vs. Confusion]

-Tx = Thiamine B1 supplement

B: [Korsakoff Psychosis] = CHRONIC PHASE! 

-Amnesia compensated with Comnfabulation 


A: Brain uses _____ metabolism intaking [___% Cardiac Output] and [____% O2 consumption] 

B: Describe pathogenic course once Cerebral ischemia occurs (2)

C: Which brain cells are most ischemia sensitive? (4)

D: Which brain cells have variable ischemia sensititvity (3)

A: Brain uses Aerobic metabolism intaking [20% Cardiac Output] and [15% O2 consumption]. 

Brain has NO O2 reserve = SENSITIVE TO ISCHEMIA

B: Post cerebral ischemia --> [Normal for 8-10 seconds] --> [Irreversible Damage AFTER 6-8 minutes!]

C: Neurons > Oligodendrocytes > [Endothelial Cells] > Astrocytes


1. Cerebellar Purkinje  

2. [(SHC-Sommer's Hippocampus CA1) Pyramidal neurons (long term memory)

3. [Cortex Watershed Layers 3 & 5] Pyramidal neurons (-->Laminar Necrosis if pt survives Global ischemia longer than 3 days)


A: What type of pathology makes up the lesser porition of Stroke cause? Describe its etiologies (2)

A: Intracranial Hemorrhage makes up 15% of causes of Stroke (Cerebral Ischemia is most common)

-Intraparenchymal Hemorrhage (HTN vs. amyloid)

-SubArachnoid Hemorrhage (Saccular Aneurysms vs. AVM)


A: Brain Histology post Global Cerebral Ischemia (3)

B: When do these Histological changes occur?


-[Red Dead Neurons] (neuronal cytoplasm appears red because necrosis attracts eosinophilia)

-DEC Nissl substance

-Dark Pyknotic nuclei

B: [6-12 hours post insult]


What type of Necrosis most likely occurs in the Watershed Areas of the Cortex?

B: Describe these Watershed Infarcts

Laminar Necrosis of

[Cortex Watershed Layers 3 & 5] Pyramidal neurons

---->Laminar Necrosis if pt survives Global ischemia longer than 3 days

B: Wedge-shaped areas of hyperemia and softening (particularly in ACA and MCA Watershed Zones)


A: Ischemic stroke --> what kind of neuro deficits? 

A2: Where do [In-Situ Thrombotic strokes] typically occur?

B: [Small Vessel SubCortical infarct] occurs from _____ (embolism or thrombosis). What's the MOD of Lacunar Stroke?

C: Describe Lacunar Syndrome (2)


A: Ischemic Stroke --> Focal neuro deficits (In-Situ Thrombotic vs. Embolic)

A2: Thrombotic= [Bifurcation of Internal Carotid and MCA]

B: [Small Vessel SubCortical infarct] occurs from [In-Situ Thrombosis] (Large Vessel Dz can be Thrombosis or embolism)

lenticulostriate vessels perfuse [BTIPC]

1) Lacunar Stroke= ischemia of lenticulostriate vessels -->  [cystic infarcts < 1.5 cm (mostly seen with MRI)] --> Lacunar Syndrome (listed below)

1A: [Internal Capsule/Pons/Corona Radiata] Stroke--> pure Motor stroke (ataxia vs. hemiplegia vs. clumsy hand)

1B: ThalamuS Stroke --> pure Sensory stroke

1C: Basal Ganglia - not included in Syndrome

Note: Lacunar lesions may be WITHOUT sx


A: Describe the Radiographic finding below

B: Clinical Presentation (3)

A: MRI Brain: 

Ischemic hemispheric infarct of the [MCA territory] --> Midline shift


1) CTL [Hemiparesis / Hemisensory loss/ Visual field deficits] affecting lower face and UE > leg

2) Hemisphere infarct will be associated with [CTL expressive aphasia] 

3) [Non-involved hemisphere ipsilateral neglect syndrome]


A: What 2 factors are the Gross & Micro findings post Ischemic infarction dependent on? 

B: Describe the Gross findings of the brain from an Acute Ischemc Infarct (3)

C: What pathology is shown in the image below? Describe its features (3)

A: [Time after insult (acute vs. subacute vs. remote)] and [Embolic(red) vs. Thrombotic(pale)] 

B: Brain Image on L

1) Swelling / softening / pallor of brain parenchyma

2) Indistinct border

3) Blurring of Cortex/DEC White matter differentiation

C: SUBAcute Ischemic Infarct = [More Distinct Borders] + [Tissue Liquification] + [Early PMN & Late macrophages/vascular proliferation]


What type of Cerebral Infarct is depicted in image?

Remote MCA Infarct (will have cystic spaces)



A: What type of Cerebral Infarct is depicted in image?

B: Features of this infarct (3)

C: Which artery is most commonly responsible for this type of infarct? 


Embolic Infarct 

1) [Usually smaller & centered at gray-white jxn] 

2) Can be single or multiple

3) May involve more than 1 vascular territory


D: Can occlude Large Artery at origin OR [occlude Large Artery and then embolize to [Distal Large A.]


A: What type of Infarct is depicted in image?

B: typical size of infarct

C: Where does this infarct (5)

D: Cause (2)

Lacunar Infarct 

B: small (no more than 1.5 cm) and cystic


[(Basal Ganglia) /Thalamus / Internal Capsule/ Pons / Corona Radiata which all = SubCortical White Matter)] 


1) HTN (Arterial Hyalinosis)

2) [small vessel dz]


A: Hemorrhagic Infarctions are usually ______ in nature

Intracranial hemorrhage

B: Name the common cause of [Above Arachnoid] Intracranial hemorrhage. List 2 examples. 

C: List the 2 Types of [BELOW Arachnoid] Intracranial hemorrhage and what their caused by 

A: Hemorrhagic Infarctions are usually Embolic in nature

Intracranial hemorrhage

B: Above Arachnoid: Traumatic causes (Epidural and SubDural Hematomas)

C: BELOW Arachnoid: Cerebrovascular Dz is cause

-SubArachnoid Hemorrhage (usually from Aneurysms)

-Parenchymal Hemorrhage (usually from HTN)


A: List the Common Locations for [Parenchyma HTN Hemorrhages] (4)

B: Which vessels contribute to [Parenchymal HTN Hemorrhages] and is associated with [Pseudoaneurysm Rupture]? (3)

What is the name of this particular phenomena? 


1. Putamen

2. Thalamus

3. Pons

3. Cerebellum

B: [Charcot Bouchard]:

1. Lenticulostriate arteries

2. Paramedial pontine vessels

3. Short circumferential vessels of Cerebellum & white matter 

similar distribution as lacunar infarcts. Histo with minimal tissue necrosis but does have cystic spaces containing macrophage-laden hemosiderin


Cerebral Ischemia manifestation varies based on Age Of InfarctDescribe...


A: Time period

B: Gross (2)

C: Micro (2)

A: 6 - 48 hours

B: [pale, soft , swollen] + [indistinct border/blurred grey-white junction]


1. 6-48 hours= [Dead Red Neurons] + Pallor Edema

2. 1-3 Days= Neutrophil infiltration + Necrosis


Cerebral Ischemia manifestation varies based on Age Of InfarctDescribe...


A: Time period

B: Gross (5)

C: Micro (3)

A: [2 days - 3 Weeks]

B: Gelatinous / Friable / Distinct Border / [Tissue liquefaction] / [Glial Scar ( >2 weeks)]


[early neutrophils]--> [macrophages in 3-5 days] ---> [vascular proliferation & reactive gliosis in 1-2 weeks]


Cerebral Ischemia manifestation varies based on Age Of InfarctDescribe...


A: Time period

B: Gross (3)

C: Micro (2)

A: [ > 3 Weeks]

B: Cystic / [+/- Hemosiderin staining] / [2° Degeneration]


-[Astrocytic Gliosis]

-[Residual Macrophages]


A: Causes of [SAHSubArachnoid Hemorrhage] (4)

B: Labs

C: [SAH​- SubArachnoid Hemorrhage] MOD

D: [Berry Saccular Aneurysm] MOD

E: What 3 Dz's are [Berry Saccular Aneurysm] associated with?


"[AnTi AA] led me straight to the SAH"


-Aneurysm (Berry Saccular Aneurysm) = COMMON NON-TRAUMATIC CAUSE




B: CSF with xanthochromia (yellow hue from bilirubin)

C: "Berry-like" thin-walled (no media) outpouchings from arterial branch points --> Rupture at the dome --> Global Vascular spasm --> Global cerebral ischemia

D: Outpouching of [Circle of Willis: ANT Communicating Artery] 2º to [Tunica media congenital defect]---> Rupture at the dome --> SubArachnoid Hemorrhage =  50% Fatality within first 24 hours, but most are asx until rupture

-[Auto Dom Polycystic Kidney Dz]




Intraventricular Hemorrhage

A: Demographic

B: Where does the Hemorrhage occur

A: Premature Infants (RARE IN ADULTS)

B: Germinal Matrix beneath ependyma(easily ruptures into ventricles)