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NBS > Week 3 > Flashcards

Week 3 Flashcards

1
Q

left vs right

corpus callosum

A

Corpus callosum: largest pathway that connects both hemispheres

Left: mainly speech processing

right: spatial

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2
Q

split brain effect

what is it

A
  • Split-brain effects: corpus callosum is lesioned
    • If you see the word face on the right side àit travels to your left side àyou are able to speak it
    • If you see the word face on the left side àit travels to your right side àyou cannot repeat the word face, but you can draw it
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3
Q

Define neural plasticity, parallel processing, neural networks, and top down vs. bottom-up processing as they pertain to cerebral cortex.

A
  • Neuroplasticity: the brain undergoes cortical organization and reorganization based on the patient’s lifestyle (i.e. blind person at birth will hear in the visual cortex)
  • Parallel processing: the ability of the brain to simultaneously process incoming stimuli of differing quality
    • MOA: The brain divides what it sees into components of color, motion, shape, and depth àthis is then analyzed independently and compared to stored memories in the visual association cortex àallows you to identify the object
    • Ex: Where (spatial and motion perception, maps, etc.) and What (face, object recognition) pathways of visual cortex
  • Top-down (cortex-driven cognition) vs bottom-up (stimulus-driven cognition)
    • Ex: Frontal eye fields (top-down driven gaze control)
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4
Q

define

primary/seconday visual cortex

achromatopsia

alexia

akinetopsia

balint syndrom

A
  • Primary (BA 17) & secondary (BA 18/19) visual cortex
    • Primary visual cortex is involved in direct vision; Secondary visual cortex is involved in the What and Where pathways
  • Achromatopsia: color blindness
  • Alexia without agraphia (“pure alexia”): severe reading problems, but all else is intact (speech, writing)
    • Etiology: PCA stroke
  • Akinetopsia: lack of spatial motion perception
  • Balint syndrome (optic ataxia, simultanagnosia, ocular apraxia)
    • Triad of impairment: inability to view visual fields as whole, difficulty fixating eyes, inability to move hand to a specific object
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5
Q

define

prosopagnosia

topographical amnesia

visual agnosia

A
  • Prosopagnosia: inability to recognize faces
  • Topographical amnesia: impairment of memories for locations and space
  • Visual agnosia: inability to recognize objects (due to lesion in secondary visual cortex)
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6
Q

define

hemispatial neglect

constructional apraxia

astereogensis

R-L disoreitation

anosognosia

A
  • Hemispatial neglect: damage to one hemisphere (usually non-dominant right-sided parietal lobe) àleft-sided neglect
  • Constructional apraxia: inability to build, assemble, or draw objects
  • Astereognosis: inability to determine shape of an object by touching it
  • Right-left disorientation: inability to tell right from left
  • Anosognosia: unawareness of self
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7
Q

define

cortical deafness

auditory agnosis

amusia

wernickes

A
  • Cortical deafness: lesion to primary auditory cortex
  • Auditory agnosia: inability to understand meaning spoken words
    • Due to damage of bilateral auditory association cortex
  • Amusia: inability to process pitch
  • Wernicke’s area (parietotemporal area): comprehension of language
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8
Q

define

hemiparesis

brocas

prefrontal cortex

A
  • Hemiparesis (unilateral paralysis), apraxia (inability to make purposeful movements)
  • Broca’s aphasia: speech production
  • Prefrontal cortex: decision making, executive function
    • Ex: Phineas Gage damaged this part of his brain and lost decision making ability
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9
Q

4 frontal lobe syndromes

A
  • Akinesia-mutism: loss of initiation/motivated behavior due to superior medial lesions
  • Dysexecutive syndrome: loss of planning, flexibility, and working memory due to lesions in the dorsolateral prefrontal cortex
  • Medial-Polar syndrome: loss of social cognition/self-other; theory of mind, empathy due to medial-polar prefrontal cortex lesions
  • Orbitofrontal syndrome: loss of goal-direct behavior due to orbitofrontal cortex lesions
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10
Q

ASA and PSA syndrome

A

Anterior Spinal Artery Syndrome

  • Etiology: trauma, atherosclerosis, thromboembolic diseases
  • Signs/sx: involves anterior 2/3 of cord àweakness (corticospinal), loss of pain/temp (spinothalamic)

Posterior Spinal Artery Syndrome

  • Etiology: atherosclerosis, thromboembolic diseases, trauma
  • Signs/sx: loss of vibration and position below leve of injury (dorsal column)
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11
Q

transverse myelitis and anterior horn cell syndrome

A

Transverse Myelitis

  • Etiology: inflammation secondary to infections, vaccinations, MS
  • Signs/sx: early onset pain at level of lesion followed by deficits of all three tracts
  • Dx: CSF studies

Anterior Horn Cell Syndrome

  • Description: LMN disease
  • Etiology: spinal muscular atrophy (symmetric involvement), poliomyelitis (asymmetrical involvement)
  • Signs/sx: fasiculations (esp on tongue), decreased reflexes, hypotonia, weakness
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12
Q

Brown-Sequard Syndrome

A
  • Etiology: trauma, etc.
  • Signs/sx: ipsilateral loss of vibration/proprioception and muscle weakness, contralateral loss of pain/temp
    • LMN lesions: at the level of the lesion due to anterior horn cell disruption
    • UMN lesions: below the level of the lesion due to tract disruption
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13
Q

Central Cord Syndrome

large vs. small lesions

A
  • Description: common site is at cervical cord
  • Etiology: trauma or Arnold-Chiari malformation
  • Signs/sx:
    • Small lesion: cape like sensory loss (loss of pain and temp bilaterally), corticospinal tract dysfunctionbilaterally
    • Large lesion: bilateral loss of all tracts (sacral region may be spared due to location of sacral fibers within tracts)
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14
Q

subacute combined degeneration

tabes dorsalis

A

Subacute Combined Degeneration

  • Description: affects posterior and lateral aspect of spinal cord
  • Etiology: B12 deficiency
  • Signs/sx: bilateral weakness, bilateral loss of position/vibration

Tabes dorsalis

  • Etiology: tertiary syphilis
  • Signs/sx: bilateral loss of position/vibration (dorsal column)
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15
Q

Define aphasia

A

Inability to speak or understand previously spoken language due to a lesion in the brain

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16
Q

difference between phonation and articulation/rhythm

A
  • Phonation (production of vocal sounds)
    • Hypophonia (reduction in voice volume), aphonia (loss of voice volume)
  • Articulation/rhythm (contractions of the anatomy that alters sounds – i.e. palate, tongue)
    • Dysarthrias: cerebellar ataxia (explosive speech), foreign accent syndrome (motor/premotor cortex), etc.
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17
Q

what are 4 types of aphasia

A
  • Broca’s Aphasia: nonfluent speech production; retained ability to produce sound and preserved comprehension
  • Wernicke’s Aphasia: fluent speech pattern with impaired comprehension of language (spoken, written, naming, repetition) àanomia, agraphia, acalculia, apraxia
  • Conduction Aphasia: damage to the arcuate fasiculus àpoor repetition of what patient hears (inability to repeat sentences, digits), but patient maintains otherwise fluent speech (answers questions normally)
  • Global Aphasia: combination of damage to Broca’s and Wernicke’s area àloss of speech production and comprehension
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18
Q

Define

  • Alexia:
  • Agraphia:
  • Acalculia:
  • Anomia:
  • Apraxia:
A
  • Alexia: inability to read
  • Agraphia: inability to write
  • Acalculia: inability to calculate
  • Anomia: inability to name objects
  • Apraxia: inability to perform skilled motor movements
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19
Q

Describe prognosis of aphasia

A

Positive prognosis: younger age, left handedness, female, trauma rather than stroke

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20
Q

what is apraxia

A
  • Apraxia: Inability to carry out learned, skilled motor acts despite preserved motor and sensory systems, coordination, comprehension, and cooperation
    • Often associated with aphasia
    • Ex: brushing teeth, dressing, ambulating, using tools
    • Lesions associated with apraxia: left hemisphere (usually frontal and parietal)
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21
Q

subtypes of apraxia

A
  • Ideomotor: temporal and spatial errors affecting position in space and timing of actions
    • i.e. may use limb as object (finger to comb hair)
  • Ideational: difficult in carrying out the sequence of a multi-step action
    • i.e. making a sandwich or cup of tea
    • Etiology: seen in left MCA stroke, dementia, TBI
  • Callosal: apraxia limited to left upper extremity
    • i.e. salute, wave goodbye
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22
Q

types of memory

A
  • Motor/procedural memory: motor skills)
  • Sensory specific memory: faces, sounds, tastes
  • Semantic memory: words, objects, concepts
  • Declarative memory: specific facts, figures, dates related to events, peoples, other temporal-spatial
  • Autobiographical memory: personal episodic
  • Working memory: task-related memoranda
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23
Q

Medial-temporal lobe: limbic lobe

what is it? different lesions

A
  • Consists of the hippocampus, amygdala, parahippocampal gyrus
  • Lesions:
    • Left: loss of verbal learning and new verbal memory retention (partial amnesia)
    • Right: loss of visual learning and new memory retention → form of anterograde amnesia (partial form of anterograde amnesia)
    • Bilateral: causes profound loss of learning and new memory retention (HM patient) (global amnesia)
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24
Q

Hippocampus

fxn , MOA

A

Function: memory consolidation

MOA: receives projections from association cortices and process these inputs in dentate gyrus àback to association cortices for further consolidation

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25
Q

Diencephalic amnesia:

A
  • Secondary to Alcoholic Korsakoff syndrome (lack of Vit B1) → memory loss and confabulation prominent
  • Affects mammillary bodies, anterior thalamic nucleus, and mammillothalamic tract
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26
Q

Basal forebrain amnesia:

A

Due to rupture of anterior communicating artery aneurysm that affects nuclei and pathways → inability to remember where, when or how learn info was acquired (source amnesia)

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27
Q

four types of amnesia

anterograde, retrograde, transient, partial

A
  • Anterograde amnesia: impaired learning and consolidation of new memories due to brain damage, while memories consolidated prior to illness/injury remain intact
  • Retrograde amnesia: loss of memory acquired before onset of amnesia
    • Usually a temporal gradient back in time occurs with relative preservation of more remotely acquired memory
  • Transient global amnesia: anterograde memory loss symptoms come on suddenly and last for several hours, then clear
    • Etiology: reduced blood flow, seizures, migraines
  • Partial amnesia: partial memory loss usually due to unilateral lesions
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28
Q

White matter tracts:

A
  • Cortico-cortical: association (ipsilateral), commissural (contralateral)
    • Association bundles: connect different lobes of the brain ipsilaterally
    • Commissural: connect different lobes of the brain contralaterally
  • Projection: corticopetal (thalamocortical), corticofugal (corticospinal)
29
Q

cortical layers

A
  • 3-5 layers (Allocortex – i.e. limbic system)
  • 6 layers (Neocortex – i.e. primary motor cortex)
    • Layer III: well-developed in association cortex
    • Layer IV (reception layer): well-developed in sensory cortex
    • Layer V (output layer): well-developed in motor cortex via pyramidal cells
30
Q

Homunculus

A

Medial: legs (ACA), Lateral: face, arms, hands (MCA)

31
Q

area 4, 1, 3, 2, 8, 44/45, 17, 41/42, 6, 5/7, 22, 18/19

A
  • Area 4 (primary motor cortex), Area 3/1/2 (somatosensory cortex), Area 8 (frontal eye fields), Area 44/45 (Broca’s area), Area 17 (visual), Area 41/42 (auditory)
  • Unimodal association cortices
    • Area 6 (supplemental motor cortex/premotor cortex): “motor planning and motor routines”
    • Area 5/7 (somatosensory association cortex)
    • Area 22 (auditory association cortex): discriminate different sounds
    • Area 18/19 (visual association cortex): differentiate different visions
32
Q

Broca’s vs Wernicke’s Aphasia

A
33
Q

Gerstmann syndrome

A
  • Etiology: secondary to a lesion typically involving the left parietal lobe along the region of the angular gyrus
  • Signs: agraphia, acalculia, agnosia (finger), left-right confusion
34
Q

Anton Syndrome (cortical blindness)

A
  • Etiology: lesion involving bilateral occipital lobes
  • Signs: cortical blindness
35
Q

balint syndrome

A
  • Etiology: lesion involving parietal lobes
  • Signs: simultagnosia (inability to maintain visual attention), optic ataxia (inability to coordinate extremity movement), oculomotor apraxia (inability to perform voluntary direct eye movements)
36
Q

limbic system and it components

A
  • Description: an interface between cerebral cortex (higher sensory, motor, cognitive) and brain stem visceral-somatic effector systems, allowing expression and experience of emotions through somatic, motor, endocrine, autonomic and behavioral changes
  • Limbic system components:
    • Cortical: hippocampus, parahippocampal gyrus, cingulate gyrus
    • Subcortical: amygdala, hypothalamus, anterior thalamic nuclei
37
Q

Describe the functions of the limbic system

A

Limbic functions: olfaction (olfactory cortex), memory (hippocampal formation), emotions (amygdala), homeostasis (hypothalamus), reproduction rearing/parenting, reward systems/punishment, basic/social emotions

38
Q

Hippocampal formation ‘

what is it? input and output

A
  • Hippocampal formation consists of: hippocampus proper, dentate gyrus, and subiculum
    • Input: association cortices via entorhinal cortex and perforant pathway (info processed in dentate gyrus)
    • Output: Fimbria-fornix via subiculum àassociation cortices for memory consolidation
39
Q

Hippocampal lesions:

etiology and sx

A
  • Etiology: herpes simplex encephalitis,
  • Signs:
    • Loss of spatial memory: unable to find their way in familiar surroundings; forget where they place belongings
    • Loss of temporal memory: not oriented to date or time; forget meetings and events
    • Loss of episodic memory: unable to recall day’s activities, conversations, visitors
40
Q

amygdala

def, fxn, lesions

A
  • Definition: area of the brain that is highly connected with limbic system and plays a key role in emotions
  • Function: arousal responses, signs of fear or rage, emotional responses,
    • Inputs: association cortices
    • Outputs: other limbic system (hypothalamus, autonomic activation centers)
  • Bilateral lesion: Kluver-Bucy syndrome
    • Signs/sx: reduced aggression, hypersexuality, increased oral behavior, visual agnosia
41
Q

basal forebrain

decription and components

A
  • Description: area of the brain that plays an important role in reward processing, addictions; interconnected with amygdala, hippocampus, hypothalamus, cortex
  • Components: nucleus accumbens
42
Q

what happens when lesions

medial thalamic CVA, medial temporal sclersosis

and other disorders

A
  • Medial thalamic CVA: leads to diplopia, lethargy, hemiparesis, amnesia
  • Medial temporal sclerosis (temporal lobe epilepsy): intractable epilepsy
  • Disorders of limbic system: autism, schizophrenia, bipolar disorder, TBI, ADHD
43
Q

basal ganglia

description, fxn, dysfxn

A
  • Description: group of subcortical nuclei including: caudate, putamen, globus pallidus, subthalamic nucleus, substantial nigra
  • Function of basal ganglia: goal-directed voluntary movements (motor learning, motor pattern selection, proper initiation of movement)

Dysfunction of basal ganglia: no weakness, contralateral motor deficits, hypokinetic movements, gait disorders

44
Q

explain the nuclei and their fxn

A
  • Caudate: role in learning, memory systems, language comprehension
  • Putamen: role in regulating movement, learning
  • Globus pallidus: role in voluntary movement at subconscious level and relays info to thalamus (two parts: globus pallidus pars externa/Gpe and pars interna/Gpi)
  • Subthalamic nucleus: receives afferents from globus pallidus externa, motor cortex, and substantia nigra
  • Substantia nigra: produces dopamine
45
Q

direct pathway

A

Direct pathway: cortex releases glutamate → striatum → D1 receptor activation → GABA release to inhibit Gpi/SNr (normally inhibits thalamus) → thalamus is activated → acts on cortex → increased movement

46
Q

indirect pathway

A

Indirect pathway: cortex releases glutamate → striatum → D2 receptor activation → GABA release to inhibit Gpe (normally inhibits STN and Gpi/SNr) → STN is able to excite Gpi/SNr via gluatamate → inhibition of thalamus via GABA → thalamus is unable to act on cortex → decreased movement

47
Q

Nigrostriatal circuitry

A

Nigrostriatal circuitry: Dopamine released by SNr either excites direct pathway or inhibits the indirect pathway

48
Q

Parkinson’s Disease

patho, sx

A

Pathophysiology: loss of dopaminergic neurons of substantia nigra pars compacta → loss of direct pathway activity → decreased movement

Sx (TRAPS): Tremor, Rigidity, Akinesia, Postural instability, Shuffling gait

49
Q

levodopa and carbidopa

MOA, SE

A
  • Dopamine precursor (Levodopa)
    • MOA: Dopamine precursor given orally → absorbed in duodenum
      • Bypasses rate-limiting step of dopamine synthesis
    • Side effects: dyskinesia (abnormal involuntary movements) after long-term use, nausea, GI upset, lowers BP
      • Carbidopa (prevents peripheral breakdown of Levodopa into dopamine) is now given in combination to minimize these side effects
50
Q

essential tremor

def, patho, tx

A
  • Definition: involuntary rhythmic oscillatory movement that is associated with the movement of a muscle (i.e. postural tremor)
  • Pathophysiology: suspected GABAergic dysfunction
  • Treatment
    • Beta blockers (i.e. propranolol): first-line treatment
      • MOA: non-selective beta antagonist → decreases muscle contractility via beta-2 antagonism
      • SE: low BP, bradycardia, can mask hypoglycemia
    • Primidone (anticonvulsant): first line treatment
      • MOA: metabolized to phenobarbital and phenylethylmalonamide → reduces high frequency repetitive firing → reduction of tremor
      • SE: confusion, ataxia, nausea, sedation
51
Q

Hypokinetic

3 types aand examples

A
  • Drug-induced parkinsonism (MPTP, metoclopramide, anti-psychotics)
  • Parkinson’s disease
    • Signs/sx: decreased arm swing, blank face, chin tremor
      • TRAPS: Tremor, Rigidity, Akinesia, Postural instability, Shuffling gait
  • Parkinson’s-plus syndrome
    • Ex: Wilson’s disease, cortical basal degeneration
52
Q

multiple system atrophy or progrssive supranuclear palsy

A
  • Multiple system atrophy
    • MRI: cerebellum and pons degeneration (potine-cerebellar atrophy)
  • Progressive supranuclear palsy
    • Signs: loss of voluntary eye movement
    • MRI: midbrain atrophy –> penguin sign (small head, big belly)
53
Q

types and example of tremors

A
  • Rest (i.e. Parkinsons’s Disease) – alleviated by intention of movement
  • Postural (i.e. essential tremor (ET), physiological tremor)
    • Essential tremor: head and voice tremor are common
      • Yes-yes tremor
  • Action (i.e. essential tremor (ET), cerebellar tremor)
  • ALL (i.e. rubral tremor, long-standing PD tremor, long-standing ET)
54
Q

types and example of jerks (3)

not including rahul

A
  • Tics (may be voluntarily suppressed)
  • Chorea (dance-like; sudden, jerky, purposeless movements)
    • Ex: Huntington’s Disease, Rheumatic Fever
  • Myoclonus (sudden, brief, uncontrolled muscle contractions)
    • Ex: hiccups, renal/liver failure
55
Q

type and example of dystonia

A
  • Writer’s cramp, blepharospasm, torticollis
  • Cervical dystonia:
    • Signs: no-no tremor; tilted head
    • Tx: botox
56
Q

Subarachnoid hemorrhage (SAH)

etiology, patho, sx

A
  • Etiology: trauma, cerebral aneurysm, arteriovenous malformations, neoplasms
    • Cerebral aneurysm:
      • Types: Saccular (congenital or berry – sticking out), fusiform (bilateral vessel dilation), mycotic (fungal infection àweak vessels), traumatic, pseudoaneurysm, neoplastic
      • Location: most commonly found in anterior circulation
  • Pathophysiology: hemorrhage of vessels within the subarachnoid space
  • Symptoms: worst headache of life, nuchal rigidity, photophobia, focal neuro deficit, coma
57
Q

SAH

complications, dx, tx

A
  • Complications: elevated ICP, brain herniation, focal cerebral ischemia, vasospasm, hydrocephalus
  • Diagnosis: CT scan/MRI scan, lumbar puncture (if imaging is inconclusive – be careful regarding herniation), cerebral angiogram to determine location
  • Treatment: craniotomy, vasodilators (for vasospasms)
58
Q

IPH

etiology, patho, dx, tx

A
  • Etiology:
    • Hypertension of small vessels (i.e. lenticulo-striate vessels), neoplasm, vasculitis, reperfusion of ischemic stroke
  • Pathophysiology: chronic HTN of small vessels –> segmental weakness –> formation of Charcot-Bouchard microaneurysms –> rupture –> hemorrhage
    • Common locations: putamen, thalamus, pons, cerebellum (also: internal capsule)
  • Diagnosis: non-contrast CT scan
  • Treatment: observation, aspiration, evacuation
59
Q

amyloid angiopathy

description, patho, dx, tx

A
  • Description: recurrent, lobar disease with a preference for the occipital lobe
  • Pathogenesis: beta amyloid deposits on walls of many arteries –> weakening of arteries –>rupture and hemorrhage
    • Associated with Alzheimers
  • Dx: Congo-red stain (apple-green birefringement)
  • Tx: observation, evacuation (must be careful b/c so many deposits with possibility of rupturing)
60
Q

Traumatic Intracranial Hemorrhage

MOI and management

A
  • General mechanisms of injury:
    • Severe injury to head –> elevated ICP –> cerebral ischemia/direct vascular injury –> punctate hemorrhages (diffuse axonal injury)
  • General ICP management:
    • Elevation of head, brief hyperventilation, mannitol
61
Q

epidural hematoma

etiology, epidemiology, patho, sx

A
  • Etiology: skull fracture involving pterion
  • Epidemiology: young patients (1% amongst TBI patients)
  • Pathophysiology: rupture of middle meningeal artery
  • Sx: brief lucid interval with progressive mental status deterioration
62
Q

epidural hematoma

complication, dx, tx

A
  • Complications: rapid expansion of bleed –> elevated ICP –> mass effect –> transtentorial herniation, CN3 palsy
  • Diagnosis: CT shows lens-shaped hyperdense blood collection not crossing suture lines
  • Treatment: craniotomy
63
Q

subdural hematoma

etiology, epidemology, patho

A
  • Etiology: trauma, cerebral atrophy, old age, alcoholism, shaking babies
  • Epidemiology: old age
  • Pathophysiology: tearing of bridging veins over the convexity
64
Q

subdural hematoma

complications, dx, tx

A
  • Complications: brain herniation, focal deficit, elevated ICP
  • Diagnosis: CT scan shows crescent shaped bleed and midline shift
    • Acute (1-3 days): hyperdense on CT scan
    • Subacute (4 days – 2 weeks): isodense on CT
    • Chronic (>2 weeks): hypodense on CT
  • Tx: evacuation via craniotomy (if acute), Burr holes (if subacute, chronic), observation
65
Q

Describe the pathophysiology of altered consciousness

A

Cerebral edema → increased ICP → decreased cerebral perfusion pressure → decreased cerebral blood flow

66
Q

areas important to alertness

where to lesion

A
  • Lesions to areas that are important in consciousness (mediated by serotonin, dopamine, histamine and acetylcholine)
    • Reticular formation (brainstem) → thalamus → cortex
      • Brainstem lesion or bilateral thalamus/cortex dysfunction → LOC
        • Bi-hemisphere involvement could be due to mass effect
67
Q

Describe the Cushing reflex

A
  • Cushing reflex: Widening pulse pressure (increased BP), irregular breathing (decreased RR), and bradycardia (decreased pulse)
    • CPP = MAP - ICP
    • Mechanism: Increased ICP → decreased cerebral perfusion pressure (CPP) → increased BP to increase CPP → increased BP is sensed by carotid sinus → decreased pulse
68
Q

Describe the mechanism of herniation

A

Increased ICP → intracranial mass volume → herniation

69
Q

Describe decorticate and decerebrate posturing

A
  • Decorticate posture (arms at CORE): lesion above level of red nucleus (midbrain tegmentum)
  • Decerebrate posture (arms at side): lesion below level of red nucleus (midbrain tegmentum)

NBS (8 decks)

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